Symptoms Of Hepatic Encephalopathy Research Articles

Frequency of H. pylori in liver cirrhosis patients with overt Hepatic encephalopathy at tertiary care hospital, Karachi.

Background: Ammonia is detoxified in the liver, and hepatic insufficiency due to cirrhosis leads to raised ammonia, causing symptoms of Hepatic Encephalopathy (HE). Studies proclaim that Helicobacter pylori (H. pylori) accelerate ammonia production. The study objective was to establish the frequency of H. pylori in liver cirrhosis patients with overt HE.
 Methodology: This cross-sectional study was conducted in Medical Unit-I Abbasi Shaheed Hospital, Karachi, from May to November 2018. Liver Cirrhosis patients between the ages of 31-60 years were selected via non-probability sampling. Patients of any sex suffering from liver cirrhosis for six months, as proved by ultrasound and overt HE diagnosed using West Haven Criteria, were included in the study. Stool samples were collected from patients in a sterile manner. Results of stool for H. pylori antigen were recorded. Data were analyzed using SPSS version 16.0.
 Results: Out of 135 patients with Liver Cirrhosis with overt HE, 42 (31.1%) suffered from H. pylori infection while 93 (68.9%) patients did not. The mean age of patients was 44.14 ± 8.49 years. Stratification of the age of patients with H. pylori infection showed significant results (p=0.00). The mean disease duration was 4.72 ± 1.24 years. Stratification based on disease duration with H. pylori infection revealed significant results (p=0.00). Stratified findings based on Child-Pugh classification and H. pylori infection were insignificant (p=0.50).
 Conclusion: Our study reveals there is less frequency of H. pylori infection amongst liver cirrhotic patients. However, amongst those infected, many had a longer duration of disease. Our study indicates more cases of H. pylori infection with increasing age of liver cirrhosis patients. Furthermore, the relation between H. pylori infection and the Child-Pugh classification indicates that overt HE may be attributed to factors other than H. pylori infection.

Outcomes of transjugular intrahepatic portosystemic shunt using 12 mm diameter polytetrafluoroethylene covered stents in cirrhotic patients with portal hypertension.

PURPOSE We aimed to evaluate the safety and efficacy of 12 mm diameter polytetrafluoroethylene (PTFE)- covered stents for the creation of transjugular intrahepatic portosystemic shunt (TIPS) in cir- rhotic patients with portal hypertension complicated by variceal bleeding and volume-overload. METHODS This retrospective study included 360 patients who had TIPS created between January 2004 and December 2017 using 12 mm diameter PTFE-covered stents. Demographic data, model for end- stage liver disease (MELD) score, etiology of cirrhosis, and Charlson comorbidity index were recorded. Symptoms of hepatic encephalopathy (HE), variceal re-bleeding, improvement in vol- ume-overload, TIPS revisions and the need for intervention, and overall survival were assessed. RESULTS The mean age of the patients was 56.8 ± 9.9 years, and the technical success rate was 99.4%. The rates of improvement of volume-overload post-TIPS were 59.5%, 69.8%, and 81.7% at 3, 6, and 12 months, respectively. About 93.3% of patients were free from paracentesis or thoracentesis at 12 months. The rates of re-bleeding post-TIPS were 4%, 12%, and 12.9% at 3, 6, and 12 months, respectively. The rate of TIPS revision at 12 months was 6.5%. Percentage of patients with any symptoms of HE were 34.4%, 42.9%, and 49.5% at 3, 6, and 12 months, respectively. All HE were appropriately medically managed and no patients required a TIPS reduction. CONCLUSION TIPS placement using 12 mm PTFE-covered stents is efficacious in cirrhotic patients with portal hypertension complicated by variceal bleeding or refractory volume-overload, with an accept- able safety profile.

Efficacy of TIPS Reduction for Refractory Hepatic Encephalopathy, Right Heart Failure, and Liver Dysfunction.

OBJECTIVE. The purpose of this study was to determine clinical outcomes of patients undergoing TIPS reduction. MATERIALS AND METHODS. In this institutional review board-approved, HIPAA-compliant study, all TIPS reductions performed at two institutions from January 1, 2008 to January 31, 2016, were retrospectively identified. Patients were divided into two groups according to pre-TIPS symptoms: volume overload due to ascites or hydrothorax (VO; n = 14) or variceal bleeding (VB; n = 12). Patient demographics, pre-TIPS model for end-stage liver disease score, pre- and post-TIPS portosystemic gradients, and clinical parameters were recorded. The primary endpoint was change in symptoms of hepatic encephalopathy (HE; West Haven criteria), right heart failure, or liver dysfunction. Secondary endpoints included paracentesis rate for the VO group and rebleeding for the VB group. RESULTS. The degree of HE increased in 24 of 26 patients (92%) after TIPS placement and decreased in 24 of 26 patients (92%) after TIPS reduction. Mean West Haven scores for the VO group decreased after TIPS reduction (from 2.57 ± 0.97 [SD] to 1.07 ± 0.70; p < .001). Mean West Haven scores for the VB group also decreased after TIPS reduction (from 2.45 ± 0.89 to 1.27 ± 0.86; p = .007). Right heart failure improved in two of three patients (67%), and total bilirubin improved in one of three patients (33%). Follow-up data were available up to median of 134 days (interquartile range, 44-286). TIPS reduction led to an increased paracentesis rate compared with before TIPS placement in four of 14 patients with VO (29%). One patient had a stable paracentesis rate after TIPS reduction compared with before TIPS placement. Variceal rebleeding did not occur in any patients with VB after TIPS reduction. At 54 days after TIPS reduction, one of the 12 patients with VB (9%) experienced hematemesis due to an endoscopically proven band-related ulcer. CONCLUSION. TIPS reduction successfully resolved HE and refractory right heart failure in most patients. In patients with VB, TIPS reduction with variceal embolization results in a low risk of short-term recurrent VB. However, in patients with VO, ascites may return or worsen after TIPS reduction despite improvement in HE.

Hepatic encephalopathy due to a congenital portosystemic shunt: a disease with a changeable presentation.

The presence of congenital portosystemic shunts in adult patients is an uncommon entity that can manifests itself with hepatic encephalopathy symptoms. However, its clinical presentation can be very diverse and varied, hence it is essential to bear it in mind to be able to diagnose it. In this manuscript we exemplify this variability by presenting a patient with complex long-standing neurological syndrome of uncertain origin, that was finally diagnosed of portosystemic shunt. To perform a percutaneous shunt closure is recommended to achieve resolution of the clinical manifestations, as happened in our patient.

Hepatic Encephalopathy in Liver Cirrhosis: Precipitating factor and Outcome

Introduction: Hepatic encephalopathy, one of the major decompensating events of liver cirrhosis manifest as a wide spectrum of neurological or psychiatric abnormalities ranging from subclinical alterations to coma. The main aim of this study was to determine precipitants of hepatic encephalopathy (HE) and their impact on hospital stay and mortality.&#x0D; Methods: A hospital based cross-sectional study carried out in the Department of Medicine, Nepalgunj Medical College, Kohalpur from September 2018 to May 2019. Patients of liver cirrhosis with signs and symptoms of hepatic encephalopathy (HE) were enrolled in the study. Detailed history was taken with patients or patient's visitor regarding precipitating factors. Child Turcotte Pugh (CTP) class was used for assessing liver disease severity and West Haven classification was used for grading of hepatic encephalopathy.&#x0D; Results: Total patients of hepatic encephalopathy studied were 150. Among which, 114 (76%) were male and 36 (24%) were female. Mean age was 45 ± 11years. Common precipitating factors for hepatic encephalopathy identified were constipation 25.3%, Upper gastrointestinal bleed (9.3%), Spontaneous bacterial peritonitis (8%). No identifiable factor was observed in 6.7% cases. Significant relationship was noted with CTP class and grading of Hepatic encephalopathy. Hospital stay was also found longer (≥5 days) among patients having more than one precipitating factor.&#x0D; Conclusions: Early recognition of precipitants and patient education is very crucial in the management of hepatic encephalopathy. Patients having ≥ 2 precipitating factor had longer hospital stay and higher grade of hepatic encephalopathy.

Severe yellow fever in Brazil: clinical characteristics and management.

Little is known about clinical characteristics and management of severe yellow fever as previous yellow fever epidemics often occurred in times or areas with little access to intensive care units (ICU). We aim to describe the clinical characteristics of severe yellow fever cases requiring admission to the ICU during the 2018 yellow fever outbreak in São Paulo, Brazil. Furthermore, we report on preliminary lessons learnt regarding clinical management of severe yellow fever. Retrospective descriptive cohort study. Demographic data, laboratory test results on admission, clinical follow-up, and clinical outcomes were evaluated. From 10 January to 11 March 2018, 79 patients with laboratory confirmed yellow fever were admitted to the ICU in a tertiary hospital in Sao Paolo because of rapid clinical deterioration. On admission, the median AST was 7,000 IU/L, ALT 3,936 IU/L, total bilirubin 5.3 ml/dL, platelet 74×103/mm3, INR 2.24 and factor V 37%. Seizures occurred in 24% of patients, even without substantial intracranial hypertension. The high frequency of pancreatitis and rapidly progressive severe metabolic acidosis were notable findings. 73% of patients required renal replacement therapy. The in-hospital fatality rate was 67%. Patients with diabetes mellitus had a higher case fatality rate (CFR) of 80%, while patients without diabetes had a CFR of 65%. Leading causes of death were severe gastrointestinal bleeding, epileptic status, severe metabolic acidosis, necrohemorrhagic pancreatitis, and multi-organ failure. Severe yellow fever is associated with a high CFR. The following management lessons were learnt: Anticonvulsant drugs in patients with any symptoms of hepatic encephalopathy or arterial ammonia levels >70μmol/L was commenced which reduced the frequency of seizures from 28% to 17%. Other new therapy strategies included early institution of plasma exchange. Due to the high frequency of gastric bleeding, therapeutic doses of intravenous proton pump inhibitors should be administered.

Fatal neurological complication after liver transplantation in acute hepatic failure patient with hepatic encephalopathy

Liver transplantation is a current definitive treatment for those with end-stage liver disease. Hepatic encephalopathy is a common complication of hepatic failure, which can be improved and aggravated by various causes. It is important to differentiate hepatic encephalopathy from other diseases causing brain dysfunction such as cerebral hemorrhage, which is also related to high mortality after liver transplant surgery. A 37-year-old patient was presented with acute liver failure and high ammonia levels and seizure-like symptoms. Computed tomography (CT) of his brain showed mild brain atrophy, regarded as a symptom of hepatic encephalopathy, and treated to decrease blood ammonia level. Deceased donor liver transplantation was performed and liver function and ammonia level normalized after surgery, but the patient showed symptoms of involuntary muscle contraction and showed loss of pupil reflex and fixation without recovery of consciousness. Brain CT showed brain edema and bilateral cerebral infarction, and the patient died after a few days. The purpose of this case report is to emphasize the importance of preoperative neurological evaluation, careful transplantation decision, and proper perioperative management of liver transplantation in patients with acute hepatic encephalopathy.

Association of Hyponatremia and Encephalopathy in Patients with Chronic Liver Disease

&lt;p&gt;&lt;strong&gt;Objective&lt;/strong&gt;: To determine the association of hyponatremia in chronic liver disease patients with presentation of hepatic encephalopathy (HE) at Isra university Hospital Hyderabad.&lt;strong&gt;&lt;/strong&gt;&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods&lt;/strong&gt;: This study was cross sectional and carried out at medicine and gastroenterology department of Isra university Hospital Hyderabad and MMC Mirpurkhas. Study duration was from September 2015 to March 2016. All the cases with age more than 25 years, both genders after diagnosis of chronic liver disease with sign and symptoms of Hepatic Encephalopathy were selected in this study. Blood sample for serum sodium level, was send to diagnostic laboratory of the hospital. Hyponatremia was classified as: 130–135 mEqL (mild), 125–130 mEq/L (moderate) and &amp;lt; 125 mEq/L (severe). Hepatic encephalopathy was categorized according to the West Haven classification (4 grades).&lt;/p&gt;&lt;p&gt; &lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results:&lt;/strong&gt;&lt;strong&gt; &lt;/strong&gt;Total number of cases was 80. Mean age was 48 + 8.5 years. 55 (68.5%) patients were male. Majority of cases, 55 (68.5%) patients were infected with HCV. 40% patients had normal level of sodium, 25% had mild, 20% had moderate while 15% patients had severe hyponatremia. On the grading of encephalopathy, 30 (37.5%) patients had grade 1 encephalopathy while 25/(31.2%) patients had grade 2, 15/(18.8%) had grade 3 while 10 (12.5%) patients hade grade 4. The serum sodium levels significantly decreased with increasing severity of hepatic encephalopathy (P = 0.001).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion:&lt;/strong&gt;&lt;strong&gt; &lt;/strong&gt;We concluded that the hyponatremia is significantly linked with Hepatic Encephalopathy (HE) in patients having chronic liver disease (CLD).&lt;/p&gt;

Brain extracellular levels of dimethylarginines (ADMA, SDMA) and cGMP and their modulation by exogenous S-adenosylmethionine in rats with acute liver failure

Acute liver failure (ALF) instantly evokes symptoms of hepatic encephalopathy (HE), mainly attributed to hyperammonemia. Ammonia neurotoxicity is related to disturbances in the nitric oxide (NO)/cGMP pathway. The methylated derivative of L-arginine (MDALs) - asymmetric dimethylarginine (ADMA) but not symmetrically methylated arginine (SDMA) is an endogenous inhibitor of nitric oxide synthase. Elevated blood and brain ADMA was reported in HE patients and experimental animals. The question arose whether ALF evokes changes in the incorporation of the methyl donor S-adenosylmethionine (SAM) to MDALs, and how they affect cGMP accumulation. To this end, we investigated the effect of intracortical perfusion of SAM on the brain extracellular levels of ADMA, SDMA and cGMP in rats with ALF in the thioacetamide (TAA) model. Sprague Dawley rats (250–270 g) received three i.p. injections of TAA (300 mg/kg) at 24 h intervals. Bilateral microdialysis of the prefrontal cortex was carried out 24 h after the last TAA administration. SAM at 2 mM concentration in artificial cerebrospinal fluid was infused for 40 min and then the medium was changed back. The extracellular levels of ADMA and SDMA were analyzed using positive mode electrospray LC–DMS–MS/MS and cGMP was determined with cGMP enzyme immunoassay. ALF resulted in the increased extracellular levels of ADMA (by ~800%) and SDMA (by ~250%). Moreover, in ALF rats infusion of SAM decreased the ADMA and SDMA (~30%) as compared to the basal value. It seems reasonable that an excessive amount of substrate inhibited the enzymes synthesizing MDALs. On the other hand, the cGMP level did not differ between control and TAA rats. SAM increased by ~90% cGMP only in the control group, what indicates affected NO/cGMP pathway in TAA model. The study demonstrates, that ALF modulates methylation of arginine to MDALs in a manner affecting cGMP accumulation.

Spontaneous portosystemic shunts in noncirrhotic patients presenting with encephalopathy

Portosystemic shunts (PSS) are common in patients with chronic liver disease and portal hypertension, however, their occurrence in noncirrhotic individuals is likely under appreciated. Patients may present with symptoms of hepatic encephalopathy and/or gastrointestinal bleeding and undergo extensive work up for liver disease to no avail. Often, these patients suffer for years with accruing medical expenses and numerous hospitalizations related to repeated episodes of encephalopathy. The underlying cause may go undiagnosed or misdiagnosed as occult hepatic dysfunction or even a neuropsychological disorder. In many cases, abdominal CT imaging demonstrates the abnormal portosystemic connection well before it is recognized as the cause of symptoms. In this brief report, we discuss three cases presenting with symptoms of encephalopathy and report successful management with endovascular occlusion of the portosystemic shunts.

Correction of Hepatic Encephalopathy in Patients with Liver Cirrhosis in Combination with Intestinal Dysbiosis

65 patients with liver cirrhosis combined with intestinal dysbiosis have been examined; an assessment ofthe functional state of the liver, clinical manifestations of hepatic encephalopathy, neuropsychometric tests, intestinalmicrobiota has been carried out; Lactobacillus and Bifidobacterium as well as Methylsiliconic acid hydrogel were included into the complex treatment. Inclusion of these drugs in the complex treatment resulted in significantly better reduction of subjective and objective signs of cirrhosis, severity of functional and biochemical syndromes, symptoms of hepatic encephalopathy.

Endovascular Treatment of Symptomatic Intrahepatic Portosystemic Venous Shunt Using Amplatzer Vascular Plug II

Endovascular Treatment of Symptomatic Intrahepatic Portosystemic Venous Shunt Using Amplatzer Vascular Plug II Spontaneous intrahepatic portosystemic venous shunt (IPSVS) is a rare condition that implies abnormal communication between portal and systemic venous system within the liver parenchyma. It can be asymptomatic or present with symptoms of hepatic encephalopathy. We show a case of 74-year-old female patient with symptomatic IPSVS and successful endovascular treatment using Amplatzer Vascular Plug (AVP) II.

Helicobacter Pylori Infection / Hepatic Encephalopathy InterRelationship before and after its Eradication

Background and study aim: Helicobacter pylori (H. pylori) bacteria convert urea to ammonia, which has been implicated in causation of hepatic encephalopathy(HE) in patients with liver cirrhosis.The aim of this work was to assess the effect of helicobacter pylori infection and its eradication on hepatic encephalopathy. Patients and methods: From March 2010 to November 2011, in Tropical Medicine Department, Zagazig university Hospitals, 90 patients with grade 0-II hepatic encephalopathy were enrolled in the study. The patients diagnosed for hepatic encephalopathy using psychometric tests [number connection test (NCT), and circle connection test( CCT)] and Grading of the symptoms of hepatic encephalopathy was performed, they were evaluated for H. pylori infection (through detection of H. pylori stool Ag) , liver impairment, and blood ammonia concentration. A group of the H. pylori +ve patients were given eradication therapy (triple therapy: 1 wk therapy with omeprazole plus clarithromycin and tinidazole), then patients were revaluated after 2 months using psychometric tests and blood ammonia concentration and compared with untreated group. Results: In our study, the mean level of blood ammonia concentration was significantly higher in H. pylori-positive patients (group II and III: 78.1±9.36 and 82.73±12.22 mmol/L) in comparison to H. pylori-negative patients (group I: 65±17.47 mmol/L ) where P<0.001. Also the time needed to perform NCT and CCT show the lowest mean in H. pylori - negative patients (64.73±13.08 and 35.67±6.66 sec. respectively) in comparison to H. pylori- positive patients with statistically significant difference (P<0.001 for both tests). CCT was significantly reduced in treated and eradicated patients after therapy (30.46±4.9 sec) and shows statistically significant difference (P<0.001) in comparison to untreated or failed to eradicate groups. The blood ammonia concentration in patients with H pylori was significantly reduced after bacterium eradication compared with the concentration after conventional treatment to HE in H. pylori infected controls (49.04± 13.67 vs 61.17±9.81). However, blood ammonia level was reduced in those who received treatment and failed to eradicate in a significant difference from those who didn’t receive eradication therapy (infected controls) (61.17±9.81 vs 75±14.9). Also there was statistically significant difference as regard to hepatic encephalopathy grade pre- and post treatment in infected treated and eradicated group (P=0.04) while there was no statistically significant difference in infected controls or failed to eradicate groups. Conclusion: H pylori infection is an important factor for inducing high blood ammonia concentration in HE patients. Anti-H. pylori therapy results in reduction in blood ammonia levels and may be helpful for treatment and prevention of HE.

Precipitating factors of hepatic encephalopathy: An experience at Mansoura Specialized Medical Hospital, Egypt

Background/Aim: Hepatic encephalopathy (HE) is a frequent complication of liver cirrhosis, and its development heralds a poor prognosis as it is associated with shortened patients' survival. Reversibility of the precipitating factors of HE is of prognostic significance. This work was designed to study the precipitating factors of HE in patients with liver cirrhosis at Mansoura Specialized Medical Hospital, Egypt. Materials and Methods: A total of 237 consecutive known chronic liver disease patients, presented with signs and symptoms of hepatic encephalopathy, were admitted in the hepatology unit of Mansoura Specialized Medical Hospital from September 2009 to September 2010. The precipitating factors of hepatic encephalopathy were identified with the aid of clinical examination and appropriate investigations. Grades of HE and Child-Pugh scores were determined. Results: The precipitating factors of HE in our studied cases were upper GI bleeding in 87 patients (36.7%), advanced HCC in 43 patients (18.14%), infections in 37 patients (15.61%), excess protein intake in 27 patients (11.39%), electrolyte imbalance in 7 patients (2.95%), and altered bowel habits in 33 patients (13.92%). Males were commonly affected by HCC (P < 0.05) and upper GI bleeding more than female patients (P < 0.05). Male patients were commonly presented with HE (63.29%), and this gender difference reached a statistical significance among those presented with upper GI bleeding (P < 0.05) and HCC (P < 0.05). Upper GI bleeding, advanced HCC, and infections were the leading causes of death with a higher prevalence in grade IV comatose (P < 0.05), child C (P < 0.05), male patients (P < 0.05). Conclusions: Our data revealed that upper GI bleeding, advanced HCC, and infections are the main precipitating factors of HE as well as the major leading causes of death in patients with liver cirrhosis. Priority should be given to control these factors by allocation of the hospital funds, medications, and human efforts. Implementation of an effective screening program for early HCC detection all over the country should be on the top of the official health concerns.

A Blood Test for Subclinical Hepatic Encephalopathy

Minimal hepatic encephalopathy (MHE) — present in up to half of cirrhotic patients with no clinical symptoms of hepatic encephalopathy (HE) — is

Postural control in patients with liver cirrhosis: a posturographic study

Ataxia has been suggested in the literature to be a symptom of hepatic encephalopathy (HE), but so far has not been objectively quantified. In this study, we wanted to objectively quantify ataxia in patients with liver cirrhosis. One hundred and seven patients with liver cirrhosis were tested for postural control using posturography and compared with 25 controls. For quantification of HE, we used the number connection tests A and B, ammonia levels (NH3), and the partial pressure of ammonia in the arterial blood (pNH3). Patients showed an impaired postural control compared with controls. Patients with Child C cirrhosis had lower scores in the posturography than those with Child A or B cirrhosis. Patients with alcohol-induced (AIC) Child B cirrhosis achieved lower scores in the posturography than those with non-alcohol-induced (NAIC) Child B cirrhosis. Patients with AIC Child C had lower scores than the corresponding NAIC patients, although this did not reach statistical significance. In the NAIC group Child C patients, in the AIC group Child B and C patients had lower scores than the controls. Patients with abnormal results in the number connection tests, as well as those with high NH3 and pNH3 levels showed worse postural control than those with normal results. Patients with cirrhosis have an impaired postural control compared with controls and this impairment deteriorates with progression of liver disease. HE as well as past alcohol abuse contribute to the pathogenesis of ataxia in liver cirrhosis and past alcohol abuse leads to an earlier and more pronounced manifestation of ataxia in the affected patients.

Bradykinesia in cirrhotic patients with early hepatic encephalopathy is related to a decreased glucose uptake of frontomesial cortical areas relevant for movement initiation

Bradykinesia is one of the first symptoms of hepatic encephalopathy (HE). Recently it has been suggested that bradykinesia in HE is due to disturbances in movement initiation. Areas involved in self-initiated movement are the motor- and premotor cortex, the supplementary motor cortex, the motor areas of the cingulate gyrus, and part of the frontomesial- and parietal cortex. The present study aimed to test the hypothesis that bradykinesia in HE is due to a functional disturbance of these areas. Fourteen cirrhotics with grade 0-I HE were examined. Patients with alcoholic cirrhosis or concomitant cerebral disorder were excluded. Patients underwent a 3-dimensional computer-assisted movement analysis for forearm pronation and supination, hand tapping and finger tapping and a (18)F-fluorodesoxy-glucose-PET-examination during rest, analysed with statistical parametric mapping (SPM99). The frequency of finger- and hand tapping was significantly correlated to the glucose metabolism of the motor area of the cingulate gyrus and frontomedial, frontodorsal and parietal cortical areas known to be activated with self-initiated movements. A decrease of movement frequency was associated with a reduction of glucose metabolism within these areas. These data support the hypothesis that bradykinesia in cirrhotics with HE is caused by an alteration of movement initiation.

186 Is fatigue as a symptom of hepatic encephalopathy (HE) induced by early changes of cerebral adenosin A1 receptors? Investigations with F-18-CPFPX and pet techniques in cirrhotics with manifest and non-manifest HE

186 Is fatigue as a symptom of hepatic encephalopathy (HE) induced by early changes of cerebral adenosin A1 receptors? Investigations with F-18-CPFPX and pet techniques in cirrhotics with manifest and non-manifest HE

TIPS-related hepatic encephalopathy: management options with novel endovascular techniques.

Hepatic encephalopathy is a common complication that develops after creation of a transjugular intrahepatic portosystemic shunt (TIPS). Although most patients respond well to conservative medical therapy (ie, protein-restricted diet, nonabsorbable disaccharides, nonabsorbable antibiotics), a small percentage of patients (3%-7%) do not benefit from these methods and require more invasive therapeutic approaches. One option is emergent liver transplantation, but the majority of patients are not suitable candidates. Recently, various percutaneous techniques have been described that alter the hemodynamics through the shunt by occluding it with coils or balloons or by reducing its diameter by inserting constrained stents or stent-grafts. Other techniques have been used for patients with TIPS-related hepatic encephalopathy in whom spontaneous splenorenal shunts are present. In many patients with refractory hepatic encephalopathy, these percutaneous techniques have produced symptomatic improvement, with either a complete resolution or a substantial reduction in hepatic encephalopathy symptoms that can be controlled with medical therapy. Unfortunately, despite all attempts, some patients remain incapacitated and ultimately die. Further research is necessary to improve our understanding of TIPS-related hepatic encephalopathy so that newer, less invasive and safer procedures can be developed to treat this difficult clinical problem.

Effects of ammonia and hepatic failure on the net efflux of endogenous glutamate, aspartate and taurine from rat cerebrocortical slices: modulation by elevated K + concentrations

Cerebrocortical minislices derived from control rats (“control slices”) and from rats with thioacetamide (TAA)-induced hepatic failure showing moderate hyperammonemia and symptoms of hepatic encephalopathy (HE) (“HE slices”), were incubated with physiological saline in the absence or presence of 5 mM ammonium acetate (“ammonia”), at potassium ion (K +) concentrations ranging from 5 to 15 mM. The efflux of endogenous aspartate (Asp), glutamate (Glu) and taurine (Tau) to the incubation medium was assayed by HPLC. At 5 mM K +, perfusion of control slices with ammonia did not affect Glu and slightly depressed Asp efflux. Raising K + concentrations in the incubation medium to 7.5 led to inhibition of Glu and Asp efflux by ammonia and the inhibitory effect was further potentiated at10 mM K +. The inhibition was also significant at 15 mM K +. This suggests that, depression of excitatory neurotransmission associated with acute hyperammonemia is more pronounced under conditions of intense neuronal activity than in the resting state. HE moderately increased the efflux of Glu and Asp, and the stimulatory effect of HE on Glu and Asp efflux showed virtually no variation upon changing K + concentration up to 15 mM. Ammonia strongly, and HE moderately, increased Tau efflux at 5 mM K +. However, both the ammonia- and HE-dependent Tau efflux decreased with increasing K + concentration in the medium and was no longer significant at 10 mM concentration, indicating that intense neuronal activity obliterates the neuroprotective functions of this amino acid triggered by hyperammonemia.