Study on the comparative analysis of the efficacy of transmesenteric vein extrahepatic portosystemic shunt and transjugular intrahepatic portosystemic shunt in the treatment of cavernous transformation of portal vein / 中华肝脏病杂志

Objective: To compare the safety and efficacy of transmesenteric vein extrahepatic portosystemic shunt (TEPS) and transjugular intrahepatic portosystemic shunt (TIPS) in the treatment of cavernous transformation of the portal vein (CTPV). Methods: The clinical data of CTPV patients with patency or partial patency of the superior mesenteric vein treated with TIPS or TEPS treatment in the Department of Vascular Surgery of Henan Provincial People's Hospital from January 2019 to December 2021 were selected. The differences in baseline data, surgical success rate, complication rate, incidence rate of hepatic encephalopathy, and other related indicators between TIPS and TEPS group were statistically analyzed by independent sample t-test, Mann-Whitney U test, and Chi-square test. Kaplan-Meier survival curve was used to calculate the cumulative patency rate of the shunt and the recurrence rate of postoperative portal hypertension symptoms in both groups. Results: The surgical success rate (100% vs. 65.52%), surgical complication rate (6.67% vs. 36.84%), cumulative shunt patency rate (100% vs. 70.70%), and cumulative symptom recurrence rate (0% vs. 25.71%) of the TEPS group and TIPS group were statistically significantly different (P < 0.05). The time of establishing the shunt [28 (2141) min vs. 82 (51206) min], the number of stents used [1 (12) vs. 2 (15)], and the length of the shunt [10 (912) cm vs. 16 (1220) cm] were statistically significant between the two groups (t = -3.764, -4.059, -1.765, P < 0.05). The incidence of postoperative hepatic encephalopathy in the TEPS group and TIPS group was 6.67% and 15.79% respectively, with no statistically significant difference (Fisher's exact probability method, P = 0.613). The pressure of superior mesenteric vein decreased from (29.33 ± 1.99) mmHg to (14.60 ± 2.80) mmHg in the TEPS group and from (29.68 ± 2.31) mmHg to (15.79 ± 3.01) mmHg in TIPS group after surgery, and the difference was statistically significant (t = 16.625, 15.959, P < 0.01). Conclusion: The best indication of TEPS is in CTPV patients with patency or partial patency of the superior mesenteric vein. TEPS improves the accuracy and success rate of surgery and reduces the incidence of complications.

Embolización de colaterales portosistémicas espontáneas como tratamiento de la encefalopatía hepática refractaria / Embolization of spontaneous portosystemic shunts as treatment for refractory hepatic encephalopathy

BACKGROUND: Hepatic encephalopathy (HE) is a common complication of cirrhosis associated with a reduced survival. The presence of high-flux spontaneous porto-systemic shunts can induce HE even in patients with preserved liver function. AIM: To evaluate the effect of spontaneous porto-systemic shunt embolization (SPSE) over HE and its long-term evolution. MATERIAL AND METHODS: Retrospective analysis of 11 patients (91% males) with severe HE non-responsive to medical treatment in whom a SPSE was performed. The grade of HE (employing West Haven score), survival, MELD and Child-Pugh score, ammonia levels, degree of disability (employing the modified Rankin scale (mRs)) were evaluated before and at thirty days after procedure. RESULTS: The most common etiology found was non-alcoholic steatohepatitis (63.6%). A reduction of at least two score points of HE was observed in all patients after thirty days. There was a significant reduction on median (IQR) West Haven score from 3 (2-3) at baseline to 1 (0-1) after the procedure (p < 0.01). Twelve months survival was 63.6%. There was a decrease in median ammonia level from 106.5 (79-165) (ug/dL) to 56 (43-61) after SPSE (p = 0.006). The median mRS score before and after the procedure was 3 (3-5) and 1 (1-2.5), respectively (p < 0.01). Conclusions: According to our experience, SPSE is a feasible and effective alternative to improve HE and functionality of patients with refractory EH.

Cerebral hemodynamic and metabolic changes in fulminant hepatic failure / Modificações da hemodinâmica e metabolismo cerebral na insuficiência hepatica fulminante

ABSTRACT Intracranial hypertension and brain swelling are a major cause of morbidity and mortality of patients suffering from fulminant hepatic failure (FHF). The pathogenesis of these complications has been investigated in man, in experimental models and in isolated cell systems. Currently, the mechanism underlying cerebral edema and intracranial hypertension in the presence of FHF is multi-factorial in etiology and only partially understood. The aim of this paper is to review the pathophysiology of cerebral hemodynamic and metabolism changes in FHF in order to improve understanding of intracranial dynamics complication in FHF.

RESUMO O edema cerebral e a hipertensão intracraniana (HIC) são as principais causas de morbidade e mortalidade de pacientes com insuficiência hepática fulminante (IHF). A patogênese dessas complicações tem sido investigada no homem, em modelos experimentais e em sistemas celulares isolados. Atualmente, o mecanismo subjacente ao edema cerebral e HIC na presença de IHF é multifatorial em etiologia e pouco compreendido na literatura. O objetivo deste trabalho é revisar a fisiopatologia das alterações hemodinâmicas e metabólicas cerebrais na IHF, visando melhorar a compreensão da complicação da hemodinâmica encefálica na IHF.

Observational Cohort Study of Hepatic Encephalopathy After Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Abstract: Introduction and aim. Hepatic encephalopathy (HE) is a common complication of transjugular intrahepatic portosystemic shunting (TIPS). It is associated with a reduced quality of life and poor prognosis. The aim of this study was to compare two groups of patients who did and did not develop overt HE after TIPS. We looked for differences between these groups before TIPS. Material and methods. A study of 895 patients was conducted based on a retrospective analysis of clinical data. Data was analyzed using Fisher’s exact test, χ2, Mann Whitney test, unpaired t-test and logistic regression. After the initial analyses, we have looked at a regression models for the factors associated with development of HE after TIPS. Results. 257 (37.9%) patients developed HE after TIPS. Patients’ age, pre-TIPS portal venous pressure, serum creatinine, aspartate transaminase, albumin, presence of diabetes mellitus and etiology of portal hypertension were statistically significantly associated with the occurrence of HE after TIPS (p < 0.01). However, only the age, pre-TIPS portal venous pressure, serum creatinine, presence of diabetes mellitus and etiology of portal hypertension contributed to the regression model. Patients age, serum creatinine, presence of diabetes mellitus and portal vein pressure formed the model describing development of HE after TIPS for a subgroup of patients with refractory ascites. Conclusion. We have identified, using a substantial sample, several factors associated with the development of HE after TIPS. This could be helpful in further research.

Minimal Hepatic Encephalopathy in Cirrhosis- How Long to Treat?

Abstract: Introduction. Minimal hepatic encephalopathy (MHE) can reverse after short-term treatment. However, relapse rate of MHE after stopping treatment has not been studied so far. We aimed to evaluate long-term (9 months) efficacy of a short-term (3 months) treatment of MHE with lactulose/rifaximin, for maintenance of remission from MHE. Material and methods. In this prospective study, consecutive patients with cirrhosis and MHE were treated with lactulose/rifaximin for 3 months. After treatment, they were followed up for 6 months. Psychometric testing for diagnosis of MHE was performed at baseline, 3 months and 9 months. Results. Of the 527 patients screened, 351 were found eligible and tested for MHE. Out of these, 112 (31.9%) patients had MHE (mean age 55.3 years; 75% males). They were randomized to receive Rifaximin (n = 57; 1,200 mg/day) or Lactulose (n = 55; 30-120 mL/day) for three months. At 3 months, 73.7% (42/57) patients in Rifaximin group experienced MHE reversal compared to 69.1% (38/55) in Lactulose group (p = 0.677). Six months after stopping treatment, 47.6% (20/42) in rifaximin group and 42.1% (16/38) patients in lactulose group experienced MHE relapse (p = 0.274). The overt hepatic encephalopathy development rate (7.1% vs. 7.9%) and mortality rate (0.23% vs. 0%) were similar in both groups. The Child-Turcotte-Pugh score and model for end stage liver disease (MELD) scores of patients who had MHE relapse were higher compared to those who didn’t. On multivariate regression analysis, MELD score was an independent predictor of MHE relapse. Conclusion. Of the patients who became MHE negative after short-term (3 months) treatment with rifaximin/lactulose, almost 50% had a relapse of MHE at 6 months follow-up.

Complications Requiring Hospital Admission and Causes of In-Hospital Death over Time in Alcoholic and Nonalcoholic Cirrhosis Patients

BACKGROUND/AIMS: Data on the epidemiology of alcoholic cirrhosis, especially in Asian countries, are limited. We compared the temporal evolution of patterns of alcoholic and nonalcoholic cirrhosis over the last decade. METHODS: We retrospectively examined the inpatient datasets of five referral centers during 2002 and 2011. The study included patients who were admitted due to specific complications of liver cirrhosis. We compared the causes of hospital admissions and in-hospital deaths between patients with alcoholic and nonalcoholic cirrhosis. RESULTS: Among the included 2,799 hospitalizations (2,165 patients), 1,496 (1,143 patients) were from 2002, and 1,303 (1,022 patients) were from 2011. Over time, there was a reduction in the rate of hepatic encephalopathy (HE) as a cause of hospitalization and an increase in the rate of hepatocellular carcinoma. Deaths that were attributable to HE or spontaneous bacterial peritonitis (SBP) significantly decreased, whereas those due to hepatorenal syndrome (HRS) significantly increased over time in patients with alcoholic cirrhosis. However, in patients with nonalcoholic cirrhosis, hepatic failure and HRS remained the principal causes of in-hospital death during both time periods. CONCLUSIONS: The major causes of in-hospital deaths have evolved from acute cirrhotic complications, including HE or SBP to HRS in alcoholic cirrhosis, whereas those have remained unchanged in nonalcoholic cirrhosis during the last decade.

The Safety and Clinical Outcomes of Chemoembolization in Child-Pugh Class C Patients with Hepatocellular Carcinomas

OBJECTIVE: To evaluate the safety and clinical outcomes of chemoembolization in Child-Pugh class C patients with hepatocellular carcinomas (HCC). MATERIALS AND METHODS: The study comprised 55 patients with HCC who were classified as Child-Pugh class C and who underwent initial chemoembolization between January 2003 and December 2012. Selective chemoembolization was performed in all technically feasible cases to minimize procedure-related complications. All adverse events within 30 days were recorded using the Common Terminology Criteria for Adverse Events (CTCAE). The tumor response to chemoembolization was evaluated using the modified Response Evaluation Criteria In Solid Tumors. RESULTS: Thirty (54.5%) patients were within the Milan criteria, and 25 (45.5%) were beyond. The mortality of study subjects at 30 days was 5.5%. Major complications were observed in five (9.1%) patients who were all beyond the Milan criteria: two hepatic failures, one hepatic encephalopathy, and two CTCAE grade 3 increases in aspartate aminotransferase/alanine aminotransferase abnormality. The mean length of hospitalization was 6.3 ± 8.3 days (standard deviation), and 18 (32.7%) patients were discharged on the next day after chemoembolization. The tumor responses of the patients who met the Milan criteria were significantly higher (p = 0.014) than those of the patients who did not. The overall median survival was 7.1 months (95% confidence interval: 4.4-9.8 months). CONCLUSION: Even in patients with Child-Pugh class C, chemoembolization can be performed safely with a selective technique in selected cases with a small tumor burden.

Avaliação da influência da cirrose hepática e da encefalopatia hepática mínima na qualidade de vida / Assessment of the influence of liver cirrhosis and minimal hepatic encephalopathy on quality of life

RESUMO INTRODUÇÃO: A encefalopatia hepática mínima (EHM) tem sido associada a alterações na capacidade de condução de veículos, ao aparecimento da forma explícita de encefalopatia hepática e a um pior prognóstico. Contudo, o seu real impacto na qualidade de vida (QV) permanece controverso. Com o desenvolvimento das normas de aplicação e cotação da Pontuação Psicométrica da Encefalopatia Hepática (PPEH) para diagnóstico da EHM para a população portuguesa, este estudo tem como objetivo determinar o efeito desta perturbação neurocognitiva na QV dos pacientes. MÉTODOS: A amostra é composta por dois grupos: Grupo Controle (GC; n = 8) e Grupo Cirrose Hepática (GCH; n = 8). Dos oito pacientes pertencentes ao GCH, quatro revelaram presença de EHM, diagnosticada de acordo com os critérios da PPEH. A QV foi avaliada através do Medical Outcomes Study, Short Form-36 (SF-36). RESULTADOS: Em comparação com o GC, o GCH apresentou pontuações significativamente mais baixas em todos os domínios do SF-36, com exceção da sub-dimensão dor física. Quando se compara os pacientes com e sem EH não se observam diferenças significativas em nenhum dos domínios do SF-36. CONCLUSÕES: Os pacientes com cirrose hepática apresentam uma pior QV em relação aos indivíduos saudáveis; a EHM não afeta a QV. Estudos com maior número de pacientes são necessários para confirmação destes achados

INTRODUCTION: Minimal hepatic encephalopathy (MHE) has been associated with changes in the ability to drive, with the onset of the explicit form of hepatic encephalopathy and with a worse prognosis. However, the impact of MHE on quality of life (QoL) remains controversial. With the standardization of the Psychometric Hepatic Encephalopathy Score (PHES) for the diagnosis of MHE in the Portuguese population, this study aimed to determine the effect of this neurocognitive disorder on the patients' QoL. METHODS: The sample consisted of two groups: the control group (CG, n = 8) and the liver cirrhosis group (LCG, n = 8). Of the eight patients in the LCG, four presented with MHE, diagnosed according to PHES criteria. QoL was assessed using the Medical Outcomes Study, Short Form 36 (SF-36). RESULTS: Compared with the CG, the LCG had significantly lower scores in all domains of the SF-36, except for the physical pain subdomain. When patients with and without HE were compared, no significant differences were found in any of the SF-36 domains. CONCLUSIONS: Patients with liver cirrhosis have a worse QoL when compared with healthy controls; EHM does not affect QoL. Further studies with a higher number of patients are required to confirm these findings

Clinical outcomes of transjugular intrahepatic portosystemic shunt for portal hypertension: Korean multicenter real-practice data

BACKGROUND/AIMS: This retrospective study assessed the clinical outcome of a transjugular intrahepatic portosystemic shunt (TIPS) procedure for managing portal hypertension in Koreans with liver cirrhosis. METHODS: Between January 2003 and July 2013, 230 patients received a TIPS in 13 university-based hospitals. RESULTS: Of the 229 (99.6%) patients who successfully underwent TIPS placement, 142 received a TIPS for variceal bleeding, 84 for refractory ascites, and 3 for other indications. The follow-up period was 24.9+/-30.2 months (mean+/-SD), 74.7% of the stents were covered, and the primary patency rate at the 1-year follow-up was 78.7%. Hemorrhage occurred in 30 (21.1%) patients during follow-up; of these, 28 (93.3%) cases of rebleeding were associated with stent dysfunction. Fifty-four (23.6%) patients developed new hepatic encephalopathy, and most of these patients were successfully managed conservatively. The cumulative survival rates at 1, 6, 12, and 24 months were 87.5%, 75.0%, 66.8%, and 57.5%, respectively. A high Model for End-Stage Liver Disease (MELD) score was significantly associated with the risk of death within the first month after receiving a TIPS (P=0.018). Old age (P<0.001), indication for a TIPS (ascites vs. bleeding, P=0.005), low serum albumin (P<0.001), and high MELD score (P=0.006) were associated with overall mortality. CONCLUSIONS: A high MELD score was found to be significantly associated with early and overall mortality rate in TIPS patients. Determining the appropriate indication is warranted to improve survival in these patients.

Ammonia levels and the severity of hepatic encephalopathy

To evaluate the correlation between ammonia levels with the severity of HE in patients coming to the tertiary care hospital with liver cirrhosis and hepatic encephalopathy [HE]. Descriptive, analytical study. Shifa International Hospital, Islamabad, from January 2011 to February 2012. A total of 135 patients with liver cirrhosis and HE had serum ammonia levels measured on admission. The diagnosis of HE was based on clinical criteria, and its severity was graded according to the West Haven Criteria for grading of mental status. Ammonia levels were correlated with the severity of HE using Spearman rank correlation. Out of 20 patients with normal ammonia levels, 13 [65%] were in HE I-II, 6 [30%] were in grade-III, while 1 [5%] patient was in grade-IV HE. Out of 45 patients with mild hyperammonemia, 27 [60%] were in grade I-II, 12 [26%] were in grade-III and 6 [13%] were in grade-IV HE. Out of 34 patients with moderate hyperammonemia, 9 [26%] were in grade I-II, 18 [53%] were in grade-III, and 7 [20%] were in grade-IV HE. Out of 36 patients with severe hyperammonemia, 31 [86%] patients were in grade-IV HE [p < 0.001]. Ammonia levels correlated with the severity of hepatic encephalopathy. Greater the ammonia level, severe is the grade of hepatic encephalopathy

Encefalopatias: etiologia, fisiopatologia e manuseio clínico de algumas das principais formas de apresentação da doença / Encephalopathies: etiology, pathophysiology, and clinical management of some major forms of disease presentation

JUSTIFICATIVA E OBJETIVOS: As encefalopatias compõem um grupo heterogêneo de etiologias, onde a pronta e correta atuação médica direcionada à causa da doença, pode modificar o prognóstico do paciente. O objetivo deste estudo foi rever os aspectos fisiopatológicos das diferentes encefalopatias bem como seus principais fatores desencadeantes e manuseio clínico.CONTEÚDO: Foram selecionadas as mais frequentes encefalopatias observadas na prática clínica e discutir sua fisiopatologia, bem como sua abordagem terapêutica, destacando: encefalopatia hipertensiva, hipóxico-isquêmica, metabólica, Wernicke-Korsakoff, traumática e tóxica.CONCLUSÃO: Trata-se de uma complexa condição clínica que exige rápida identificação e preciso manuseio clínico com o intuito de reduzir sua elevada taxa de morbimortalidade. O atraso no reconhecimento dessa condição clínica poderá ser extremamente prejudicial ao paciente que estará sofrendo lesão cerebral muitas vezes irreversível.

BACKGROUND AND OBJECTIVES: Encephalopathies comprise a heterogeneous group of clinical conditions, in which the prompt and adequate medical intervention can modify patient prognosis. This paper aims to discuss the pathophysiological aspects of different encephalopathies, their etiology, and clinical management.CONTENTS: We selected the main encephalopathies observed in clinical practice, such as hypertensive, hypoxic-ischemic, metabolic, Wernicke-Korsakoff, traumatic, and toxic encephalopathies, and to discuss their therapeutic approaches.CONCLUSION: This is a complex clinical condition that requires rapid identification and accurate clinical management with the aim of reducing its high morbidity and mortality rates. Delay in recognizing this condition can be extremely harmful to the patient who is suffering from often irreversible brain injury.

Encefalopatía hiperamoniémica y hepatocarcinoma fibrolamelar / Hyperammonemic encephalopathy and fibrolamellar hepatocellular carcinoma

Presentamos el caso de una mujer de 22 años con hepatocarcinoma fibrolamelar agresivo, metastásico, de rápida evolución y con una rara forma de comienzo, como una encefalopatía hiperamoniémica. El hepatocarcinoma fibrolamelar es un tumor hepático raro, que se presenta en pacientes jóvenes, sin antecedentes de hepatopatía viral o cirrótica. Su etiología es desconocida, y tradicionalmente fue considerado como de mejor pronóstico que el carcinoma hepatocelular clásico.

We present the case of a young woman, 22 years old, with an aggressive form of fibrolamellar hepatocellular carcinoma. She began with the signs and symptoms of a hyperammonemic encephalopathy, an uncommon form of presentation. Fibrolamellar carcinoma is a rare liver tumor, which affects young patients without previous liver disease. Its etiology is unknown, and it has been considered as a tumor with a better prognosis than the classic hepatocellular carcinoma.

Encefalopatía hepática fulminante vinculada a hiperintensidad de la corteza cerebral en la resonancia magnética / Fulminant hepatic encephalopathy vinculated with hyperintensity of the cerebral cortex in magnetic resonance

Background: The presence of manganese deposits in basal ganglia is an expression of chronic liver damage in neuroimaging, whereas diffuse edema of the white matter and hyperintensity of the internal capsule are seen in MRI in acute decompensation. In fulminant encephalopathy, changes in intensity in the cerebral cortex have been described, suggesting different pathogenic aspects. Purpose: To describe and try to interpret hyperintensities images of the cerebral cortex in fulminant hepatic encephalopathy. Case report: A 42 years old woman, with history of hyperthyroidism treated with propylthiouracil developed abdominal pain, choluria and general malaise, without fever. At admission, she had jaundice, elevated liver enzymes, and hyperammronemia of 481 ug. She developed progressive impairment of consciousness falling into a non-reactive coma with intermediate size and poorly reactive pupils, absence of oculocephalic reflexes and diminished osteotendinous reflexes, with indifferent plantar reflexes. Brain CT showed brain edema without focal lesions. The MRI showed hyperintense signal abnormalities in the fronto-parietal cortex in T2 and FLAIR with restriction in difussion sequency. She became brain dead. Comment: These exceptional images on MRI are considered an expression of cytotoxic damage, consistent with high levels of ammonium in fulminant hepatic encephalopathy. The swelling of astrocytes and cortical neurons is caused by the accumulation of intracellular glutamine, highly osmophilic, and explains the restriction on the difussion and lower values in the ADC. Interstitial edema would be part of the chronic forms by acquisition of compensatory mechanisms capable of preventing the accumulation of glutamine.

Antecedentes: La presencia de depósitos de manganeso en los núcleos basales es una expresión neuroimagenológica de daño hepático crónico, así como el edema difuso de la substancia blanca y la hiperintensidad de la cápsula interna con RM en descompensaciones agudas. En encefalopatías fulminantes se ha visualizado cambio de intensidad en la corteza cerebral, sugiriendo aspectos patogénicos distintos. Propósito: Describir e intentar interpretar imágenes hiperintensas de la corteza cerebral en una encefalopatía hepática fulminante. Caso clínico: Mujer de 42 años, hipertiroidea en tratamiento con propiltiouracilo. Consultó por dolor abdominal, coluria y compromiso del estado general, sin fiebre. Ingresó con ictericia, enzimas hepática elevadas, e hiperamonemia de 481 ug. Desarrolló progresivo compromiso de conciencia cayendo en un coma no reactivo, con pupilas de tamaño intermedio pobremente reactivas, ausencia de reflejos oculocefálicos y reflejos osteotendíneos apagados, con reflejos plantares indiferentes. TAC de cerebro mostró edema cerebral, sin lesiones focales. La RM definió áreas hiperintensas en la corteza fronto-parietal en T2 y FLAIR, que presentaban incremento de señal en la difusión. Evolucionó hasta la muerte cerebral. Comentario: Estas imágenes excepcionales en la RMson consideradas expresión de daño citotóxico, en concordancia con los altos niveles de amonio de una encefalopatía hepática fulminante. El edema de astrocitos y neuronas corticales se origina por la acumulación de glutamina intracelular, altamente osmofílica, y explica la restricción en la difusión y valores menores en el ADC. El edema intersticial, sería atributo de las formas crónicas, debido a la adquisición de mecanismos compensatorios capaces de impedir la acumulación de glutaminas.

Intrahepatic Portosystemic Venous Shunt: Successful Embolization Using the Amplatzer Vascular Plug II

A 67-year-old woman presented with memory impairment and behavioral changes. Brain MRI indicated hepatic encephalopathy. Abdominal CT scans revealed an intrahepatic portosystemic venous shunt that consisted of two shunt tracts to the aneurysmal sac that communicated directly with the right hepatic vein. The large tract was successfully occluded by embolization using the newly available AMPLATZERTM Vascular Plug II and the small tract was occluded by using coils. The patient's symptoms disappeared after shunt closure and she remained free of recurrence at the 3-month follow-up evaluation.

Thioacetamide-Induced acute hepatic encephalopathy in rat: behavioral, biochemical and histological changes

As a serious neuropsychiatric disease, hepatic encephalopathy [HE] is a clinical condition with several types regarding chronicity and clinical diversity that can develop as a complication of both acute and chronic liver failure. This study evaluates changes in thioacetamide [TAA]-induced acute hepatic encephalopathy [AHE] in rat as an animal model. Both genders of C57BL6, BALB/C mice and Sprague Dawley rats; [10 animals in each group] were compared for induction of AHE to clarify which animal and gender were appropriate. The animals [10 male rats in each group] were categorized in 4 groups according to the dose of the TAA administered [200, 300 and 400 mg/kg of TAA at 24 h intervals for 4 days]. A control group was treated with solvent of TAA which was water [5 ml/kg/day]. The behavioral, biochemical markers of hepatic failure and histological aspects of thioacetamide [TAA] induced AHE and the correlation between the clinical severity and liver failure biomarkers were evaluated. Rat was shown to be an animal model of choice for AHE while the optimum dosage of TAA to induce AHE was 300 mg/kg/day at 24 h intervals for 4 days. The behavioral score was partially correlated with the rising of some biomarkers and pathological findings. Rat can be introduced as the animal of choice for AHE to study the pathophysiology, pharmacology and the survival rate of disease in liver transplant patients

Shunts portosistémicos espontáneos en pacientes con encefalopatía hepática / Spontaneous portal-systemic shunts in hepatic encephalopathy patients: preliminary experience

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome caused by hepatic dysfunction and portosystemic shunting of the intestinal blood. For HE patients nonresponsive to standard therapy, the presence of large spontaneous portal-systemic shunts can occasionally be the cause of the problem. Objective: To assess the prevalence of portal-systemic shunts in patients with cirrhosis and recurrent or persistent HE. Patients and Methods: Ten patients with liver cirrhosis were analyzed who repeatedly developed HE despite pharmacotherapy. Also, we studied seven control patients with cirrhosis and no HE, who were considered the control group. Results: Large spontaneous portal-systemic shunts were detected in all patients with HE and none in the control group (X2 13.1; P: 0.0003). If only splenorenal shunts are considered, the difference is also significant (X2 5.69; p: 0.017). Conclusion: Our study confirmed that the presence of large spontaneous portal-systemic shunts is frequent in patients with cirrhosis and recurrent or persistent HE.

La encefalopatía hepática (EH) es un síndrome neuropsiquiátrico causado por insuficiencia hepática o presencia de shunts portosistémicos (SPS) intra o extrahepáticos. En pacientes con EH refractaria a tratamiento médico habitual se ha planteado que la presencia de SPS podría ser la causa del problema. Objetivo: Evaluar la prevalencia de SPS espontáneos extrahepáticos en pacientes con cirrosis y EH recurrente o persistente. Pacientes y Métodos: Se evaluaron 10 pacientes con EH recurrentes o persistente. También, se estudiaron 7 pacientes con cirrosis y sin EH que se consideraron como grupo control. Resultados: Todos los pacientes con EH recurrente o persistente presentaron SPS; 7 presentaron shunts esplenorrenales espontáneos y 3 presentaron presencia de la vena umbilical recanalizada. Ningún paciente en el grupo control presentó SPS (X2 13,1; p: 0,0003). Si se considera sólo los shunts esplenorrenales, la diferencia también es significativa (X2 5,69; p: 0,017). Conclusión: En nuestros pacientes con cirrosis y EH recurrente o persistente fue frecuente la presencia de SPS espontáneos.

Infecciones bacterianas en el paciente cirrótico / Bacterial infections in patients with cirrhosis

Las infecciones bacterianas constituyen una complicación frecuente y severa en pacientes cirróticos debido a la existencia de alteraciones inmunológicas diversas, traslocación bacteriana y una mayor respuesta inflamatoria. La producción aumentada de citoquinas proinflamatorias, óxido nítrico y otros mediadores favorece el desarrollo de otras complicaciones, tales como deterioro hemodinámico, insuficiencia renal y encefalopatía hepática. Los efectos hemodinámicos de los mediadores inflamatorios son capaces de acentuar las alteraciones de la circulación sistémica y renal propias de la cirrosis. La insuficiencia renal en pacientes con sepsis no relacionada a peritonitis bacteriana espontánea tiene mal pronóstico incluso en casos reversibles y el índice MELD pareciera ser un buen predictor en este sentido. Estudio recientes sobre encefalopatía hepática sugieren que la respuesta inflamatoria y sus mediadores pueden ser importantes en la modulación de los efectos del amonio sobre el cerebro en los pacientes con cirrosis. El diagnóstico y tratamiento oportuno de la infección permiten mejorar el pronóstico en estos pacientes. La relación entre infección y hemorragia digestiva es estrecha, fundamentando el uso de antibióticos profilácticos. El uso de albúmina en cirróticos con infecciones diferentes a peritonitis bacteriana espontánea no ha demostrado reducir la incidencia de insuficiencia renal ni la mortalidad.

Bacterial infections are a frequent and severe complication in cirrhotic patients due to the existence of multiple immune alterations, bacterial translocation and increased inflammatory response. Increased production of proinflammatory cytokines, nitric oxide and other mediators promotes the development of other complications such as hemodynamic deterioration, renal failure and hepatic encephalopathy. Hemodynamic effects of inflammatory mediators are able to increase changes of systemic and renal circulation, typical of cirrhosis. Renal failure in patients with sepsis unrelated to spontaneous bacterial peritonitis has a poor prognosis, even in reversible cases; MELD score might be a good predictor in this regard. Recent studies about hepatic encephalophaty suggest that inflammatory response and its mediators may be important in modulating the effect of ammonia on the brain of the cirrhotic patient. Early diagnosis and treatment of the infection can improve the prognosis in these patients. The relationship between infection and gastrointestinal bleeding is narrow, justifying the use of prophylactic antibiotics. The administration of albumin to patients with cirrhosis and infections other than spontaneous bacterial peritonitis has not shown to reduce the incidence of renal failure or mortality.

A new experimental model for acute hepatic failure in rats / Novo modelo experimental em ratos para insuficiência hepática aguda

PURPOSE: To develop a reliable surgical model of acute hepatic failure and hyperammonemia in rats that avoids porto-systemic shunt and bile duct ligation, applicable to hepatic encephalopathy research. METHODS: The pedicles of right lateral and caudate lobes were exposed and clamped. One hour later, the animal was reopened, clamps were released and anterior subtotal hepatectomy (resection of median and left lateral lobes) was performed, comprising 75 percent of liver removal. Four hours after hepatectomy, blood samples and liver tissues were collected from ALF and control groups. RESULTS: Differences between ALF and control groups were significant for ALT, AST, total and direct bilirubin, sodium, potassium, alkaline phosphatasis, gamma-glutamyltransferase and most important, ammonia. Histologically, significant differences were noticed between groups. CONCLUSION: The model is useful for the study of specific aspects of ALF and the development of new therapeutic approaches.

OBJETIVO: Desenvolver um modelo cirúrgico de IHA e hiperamonemia em ratos, que evita o shunt porto-sistêmico e a ligadura do ducto biliar, que seja aplicável à pesquisa de encefalopatia hepática. MÉTODOS: Após anestesia geral e laparotomia mediana, os pedículos dos lobos laterais direito e caudado foram isolados e clampeados. Após 1 hora, o animal foi reaberto, os clampes retirados e foi realizada hepatectomia anterior subtotal (ressecção dos lobos médio e lateral esquerdo), compreendendo a remoção de 75 por cento do parênquima. Quatro horas após a hepatectomia, amostras de sangue e tecido hepático foram coletadas nos grupos IHA e controle. RESULTADOS: Diferenças entre os grupos IHA e controle foram significativas para ALT, AST, bilirrubina total e direta, sódio, potássio, fosfatase alcalina, gama glutamiltransferase e principalmente amônia. Histologicamente, diferenças significativas foram observadas entre os grupos. CONCLUSÃO: O modelo é útil para o estudo de aspectos específicos da IHA e o desenvolvimento de novas abordagens terapêuticas.