Prediction of the presence of esophageal varices using spleen stiffness measurement by transient elastography in cirrhotic patients.

BACKGROUND AND STUDY AIMS: Upper gastrointestinal endoscopy (UGE) is currently recommended in cirrhotic patients to detect the presence of esophageal varices (EV). Spleen stiffness measurement (SSM) with FibroScan has been used for this purpose, showing variable sensitivity (S) and specificity (Sp). The aim of this study was to evaluate the capability of SSM to detect the presence and size of EV in cirrhotic patients in comparison to other noninvasive modalities. PATIENTS AND METHODS: Sixty-six patients with cirrhosis who had undergone UGE in the previous 6 months underwent SSM and liver stiffness measurement (LSM) using FibroScan. Biochemical parameters and ultrasonography data were also collected to calculate other noninvasive indexes. RESULTS: Valid spleen stiffness measurements were obtained for 60 of the 66 patients initially included in the study (90.1%). In the multivariate analysis only splenomegaly and SSM were predictive of esophageal varices. SSM was the most accurate diagnostic tool, obtaining an area under the ROC curve of 0.8 for values below 48 KPascals, with S = 87%, Sp = 69%, and 76.7% of successfully diagnosed patients. CONCLUSIONS: SSM with FibroScan was significantly higher for cirrhotic patients with EV. Our study suggests that spleen stiffness may be useful to identify cirrhotic patients at risk of having EV, although further studies are needed.

[Nutrition acute pancreatitis]. / Nutrición en pancreatitis aguda.

Acute pancreatitis is a common and potentially severe disease where nutritional support does affect its development in a way it may be considered a treatment in severe cases. These include around 20% of patients and present mortality rates of 8%-39%. In mild acute pancreatitis patients are prescribed nil per os at admission and advance diet in a progressive manner the following days. Although early introduction of diet has proven to shorten the length of stay, it is still not clear when and how to introduce diet. Severe disease is a hypercatabolic situation which often appears in already malnourished patients. Early enteral nutrition has shown a significative benefit over parenteral nutrition in terms of infection rates, hyperglycemia and mortality rates. This benefit may be related to a decrease in bacterial intestinal translocation. Nasoyeyunal tube feeding is the preferred site, but there are trials supporting nasogastric tubes, a more feasible election. The following lines offer an up to date review of nutritional management in acute pancreatitis, trying to answer in a clear and practical way to the most frequent problems arising in the day to day management of this disease.

Nutrición en pancreatitis aguda / Nutrition acute pancreatitis

La pancreatitis aguda es una patología frecuente y potencialmente grave en la que el manejo nutricional influye de manera importante en su desarrollo, de tal forma que se puede considerar un tratamiento específico en los casos graves. Éstos suponen aproximadamente el 20% de los pacientes y presentan una mortalidad entre el 8-39%. En los casos leves se suele proceder a un ingreso en dieta absoluta y posterior reintroducción progresiva de la dieta. Aunque se ha demostrado que una reintroducción temprana acorta la duración del ingreso, existe incertidumbre acerca del momento y del tipo de dieta idóneos. Las pancreatitis graves son estados hipercatabólicos que se presentan en pacientes que frecuentemente presentan déficits nutricionales basales. El soporte nutricional iniciado precozmente por vía enteral ha demostrado un beneficio significativo respecto a la vía parenteral en cuanto a tasa de infección, control de glucemia y mortalidad. Este beneficio puede relacionarse con una disminución de la traslocación bacteriana. Si bien tradicionalmente se ha empleado la vía nasoyeyunal, existen estudios que apoyan la vía nasogástrica, mucho más accesible. En el siguiente texto ofrecemos una revisión actualizada del manejo nutricional en la pancreatitis aguda, intentando responder de manera clara y con un enfoque práctico a las preguntas que más frecuentemente se presentan en el manejo de esta patología (AU)

Acute pancreatitis is a common and potentially severe disease where nutritional support does affect its development in a way it may be considered a treatment in severe cases. These include around 20% of patients and present mortality rates of 8%-39%. In mild acute pancreatitis patients are prescribed nil per os at admission and advance diet in a progressive manner the following days. Although early introduction of diet has proven to shorten the length of stay, it is still not clear when and how to introduce diet. Severe disease is a hypercatabolic situation which often appears in already malnourished patients. Early enteral nutrition has shown a significative benefit over parenteral nutrition in terms of infection rates, hyperglycemia and mortality rates. This benefit may be related to a decrease in bacterial intestinal translocation. Nasoyeyunal tube feeding is the preferred site, but there are trials supporting nasogastric tubes, a more feasible election. The following lines offer an up to date review of nutritional management in acute pancreatitis, trying to answer in a clear and practical way to the most frequent problems arising in the day to day management of this disease (AU)

Masa mediastínica en paciente cirrótico / No disponible

No disponible

Profilaxis preprimaria de la hemorragia por varices / No disponible

La formación de colaterales portosistémicas, en especial en launión esofagogástrica, es una de las consecuencias más graves dela hipertensión portal. El aumento de la presión portal es la fuerzamás importante que dirige la formación de varices esofagogástricas,siendo necesario para que esto ocurra que la presión portal(estimada por el gradiente de presión venosa hepática) alcance unvalor mínimo de 10 mmHg. Posteriormente, la hiperemia esplácnicatambién contribuye al desarrollo de las varices. Las colateralesportosistémicas se forman por repermeabilización de vasospreexistentes, remodelado vascular y angiogénesis. El objetivo dela profilaxis preprimaria es evitar o retrasar la formación de varicesesofagogástricas. En modelos experimentales de hipertensiónportal, la administración precoz de vasoconstrictores esplácnicoscomo los beta-bloqueantes, de inhibidores de la síntesis de óxidonítrico o de sustancias anti-angiogénicas, inhibe la formación decolaterales portosistémicas. Sin embargo, los ensayos clínicos conbeta-bloqueantes realizados en pacientes con cirrosis sin varicescon objeto de retrasar su formación no han alcanzado los resultadosesperados

Portosystemic collateral formation, particularly at the gastroesophagealjunction, is a most serious consequence of portal hypertension.Increased portal pressure is the most significant forceunderlying gastroesophageal variceal formation, to which endportal pressure (estimated from the hepatic venous pressure gradient)must reach at least 10 mmHg. Subsequently, splanchnic hyperemiaalso contributes to variceal development. Portoystemiccollaterals result from repermeabilization of pre-extant vessels,vascular remodeling, and angiogenesis. The goal of pre-primaryprophylaxis is preventing or delaying the formation of gastroesophagealvarices. In experimental models of portal hypertension,early administration of splanchnic vasoconstrictors such as betablockers,nitric oxide synthesis inhibitors, or antiangiogenic substancesinhibits portosystemic collateral formation. However, clinicaltrials of beta-blockers in patients with cirrhosis and no varicesto delay variceal formation have failed to yield expected results (AU)

[Pre-primary prophylaxis of variceal bleeding]. / Profilaxis preprimaria de la hemorragia por varices.

Portosystemic collateral formation, particularly at the gastroesophageal junction, is a most serious consequence of portal hypertension. Increased portal pressure is the most significant force underlying gastroesophageal variceal formation, to which end portal pressure (estimated from the hepatic venous pressure gradient) must reach at least 10 mmHg. Subsequently, splanchnic hyperemia also contributes to variceal development. Portoystemic collaterals result from repermeabilization of pre-extant vessels, vascular remodeling, and angiogenesis. The goal of pre-primary prophylaxis is preventing or delaying the formation of gastroesophageal varices. In experimental models of portal hypertension, early administration of splanchnic vasoconstrictors such as beta-blockers, nitric oxide synthesis inhibitors, or antiangiogenic substances inhibits portosystemic collateral formation. However, clinical trials of beta-blockers in patients with cirrhosis and no varices to delay variceal formation have failed to yield expected results.