Hypertonic saline solution decreases oxidative stress in liver hypothermic ischemia.

BACKGROUND: Liver ischemia reperfusion injury is still an unsolved problem in liver surgery and transplantation. In this setting, hypothermia is the gold standard method for liver preservation for transplantation. Hypertonic saline solution reduces inflammatory response with better hemodynamic recovery in several situations involving ischemia reperfusion injury. Here, we investigated the effect of hypertonic saline solution in hypothermic liver submitted to ischemia reperfusion injury. METHODS: Fifty male rats were divided into 5 groups: SHAM, WI (animals submitted to 40 minutes of partial warm liver ischemia and reperfusion), HI (animals submitted to 40 minutes hypothermic ischemia), HSPI (animals submitted to hypothermic ischemia and treated with 7.5% hypertonic saline solution preischemia), and HSPR (animals submitted to hypothermic ischemia and treated with hypertonic saline solution previously to liver reperfusion). Four hours after reperfusion, the animals were euthanized to collect liver and blood samples. RESULTS: Aspartate aminotransferase and alanine aminotransferase, histologic score, and hepatocellular necrosis were significantly decreased in animals submitted to hypothermia compared with the warm ischemia group. Malondialdehyde was significantly decreased in hypothermic groups with a further decrease when hypertonic saline solution was administrated preischemia. Hypothermic groups also showed decreased interleukin-6, interleukin-10, and tumor necrosis factor-α concentrations and better recovery of bicarbonate, base excess, lactate, and glucose blood concentrations. Moreover, hypertonic saline solution preischemia was more effective at controlling serum potassium concentrations. CONCLUSION: Hypertonic saline solution before hypothermic hepatic ischemia decreases hepatocellular oxidative stress, cytokine concentrations, and promotes better recovery of acid-base disorders secondary to liver ischemia reperfusion.

NUTRITIONAL SUPPORT FOR FULMINANT HEPATITIS.

INTRODUCTION: fulminant hepatitis (FH) is associated with exacerbated hypercatabolism, hypoglycemia and hyperammonemia that are accompanied by the release of proinflammatory cytokines and catabolic hormones into the systemic circulation worsening patient's clinical condition. Nutritional support is a crucial element for the recovery of these patients. OBJECTIVES: the aim of this review is to update Nutritional Support for Fulminant Hepatitis. METHODS: the review was performed using electronic search on Medline-PubMed using Mesh-terms. RESULTS AND DISCUSSION: there are not many data available on nutritional support to fulminant hepatitis or acute liver failure. Strategies for initial nutritional intervention are focused on the control of the previously described FH metabolic derangements, and should be individualized according to the severity of patient's clinical condition. Energy and protein can be provided in amounts of 25­40 kcal/kg/day and 0.8-1.2 g/kg/day, respectively. Enteral nutrition therapy is indicated for patients with advancing encephalopathy or for those who cannot be properly fed orally. Euglycemia must be achieved and protein intake can be based on BCAA formulae. Lipids can be administered as energy supplementation with caution. Adequate nutrition therapy can potentially reduce morbidity and mortality of FH patients.

Introducción: la hepatitis fulminante se asocia a un exacerbado hipercatabolismo, la hipoglicemia y la hiperamonemia están acompañadas por la liberación de citocinas proinflamatorias y hormonas catabólicas en la circulación sistémica, empeorando la condición clínica del paciente. El apoyo nutricional es un elemento crucial para la recuperación de estos pacientes. Objetivos: el objetivo de esta revisión es actualizar el apoyo nutricional para la hepatitis fulminante. Métodos: la revisión se llevó a cabo mediante la búsqueda electrónica en Medline-PubMed, utilizando malla de términos. Resultados y discusión: no hay muchos datos disponibles sobre el apoyo nutricional para lahepatitis fulminante o fallo hepático agudo. Las estrategias de intervención nutricional inicial se centran en el control de los trastornos metabólicos de la hepatitis fulminante descritos anteriormente, que deben ser individualizadas de acuerdo a la gravedad de la situación clínica del paciente. Energía y proteína se pueden proporcionar en cantidades de 25­40 kcal / kg / día y 0,8-1,2 g / kg / día, respectivamente. La terapia nutricional enteral está indicada en pacientes con encefalopatía avanzada o para aquellos que no pueden ser adecuadamente alimentados por vía oral. Se debe obtener una euglicemia y la ingesta de proteínas puede estar basada en fórmulas de BCAA. Los lípidos se pueden administrar como suplemento energético con precaución. Una terapia nutricional adecuada puede potencialmente reducir la morbilidad y la mortalidad de los pacientes con hepatitis fulminante.

Surgical site infections in liver transplant recipients in the model for end-stage liver disease era: an analysis of the epidemiology, risk factors, and outcomes.

In recipients of liver transplantation (LT), surgical site infection (SSIs) are among the most common types of infection occurring in the first 60 days after LT. In 2007, the Model for End-Stage Liver Disease (MELD) scoring system was adopted as the basis for prioritizing organ allocation. Patients with higher MELD scores are at higher risk for developing SSIs as well as other health care-associated infections. However, there have been no studies comparing the incidence of SSIs in the pre-MELD era with the incidence in the period since its adoption. Therefore, the objectives of this study were to evaluate the incidence, etiology, epidemiology, and outcomes of post-LT SSIs in those 2 periods and to identify risk factors for SSIs. We evaluated all patients who underwent LT over a 10-year period (2002-2011). SSI cases were identified through active surveillance. The primary outcome measure was an SSI during the first 60 days after LT. Risk factors were analyzed via logistic regression, and 60-day survival rates were evaluated via Cox regression. We evaluated 543 patients who underwent LT 597 times. The SSI rates in the 2002-2006 and 2007-2011 periods were 30% and 24%, respectively (P = 0.21). We identified the following risk factors for SSIs: retransplantation, the transfusion of more than 2 U of blood during LT, dialysis, cold ischemia for >400 minutes, and a cytomegalovirus infection. The overall 60-day survival rate was 79%. Risk factors for 60-day mortality were retransplantation, dialysis, and a longer surgical time. The use of the MELD score modified the incidence and epidemiology of SSIs only during the first year after its adoption. Risks for SSIs were related more to intraoperative conditions and intercurrences after LT than to a patient's status before LT.