Isquemia hepática aguda tras hemorragia digestiva alta por varices esofagogástricas / Acute liver ischaemia after gastro-oesophageal variceal bleeding

INTRODUCCIÓN: La hemorragia digestiva alta por varices esofagogástricas (HDA por VEG) puede desencadenar una isquemia hepática aguda (IHA). El objetivo de este estudio fue analizar la incidencia de IHA tras una HDA por VEG, los factores de riesgo y su mortalidad. PACIENTES Y MÉTODOS: Estudio retrospectivo sobre pacientes cirróticos con HDA por VEG. Se clasificaron en 2 grupos, determinados por el desarrollo o no de una IHA. Definimos IHA como AST y ALT por encima de 10 veces el valor basal, descartando otras causas de hepatitis aguda. El tratamiento inicial estándar fue soporte hemodinámico, endoscopia urgente con ligadura con bandas y/o escleroterapia, somatostatina y antibióticos. En caso de fracaso de estas medidas, se recurrió a la implantación de una derivación portosistémcica percutánea intrahepática (DPPI). Ambos grupos (IHA y no-IHA) fueron comparados. RESULTADOS: Durante un periodo de 5 años, se recogieron 68 pacientes con HDA por VEG. La incidencia de IHA fue del 16,2%. Tras el análisis univariante, los factores asociados con IHA fueron la diabetes mellitus (OR: 7,5; IC: 1,9-29), shock (OR: 8,5; IC: 2,06-34) y la persistencia de la hemorragia (OR: 9, IC: 1,6-49, p = 0,03). En el análisis multivariante solo mostraron significación estadística la diabetes mellitus (OR: 8,61; IC: 1,4-52,5) y el shock (OR: 7,58; IC: 1,26-45,51). La mortalidad del grupo de IHA fue mayor (45%) que en el grupo no-IHA (10,5%) (p = 0,012). CONCLUSIONES: La IHA tras una hemorragia digestiva por VEG en el paciente cirrótico ocurrió en el 16,2%, asociándose con un peor pronóstico y una mortalidad del 45%. Nuestros resultados sugieren que la diabetes mellitus y el shock hipovolémico son factores de riesgo para el desarrollo de IHA. La detección precoz de estos pacientes en riesgo podría por tanto ayudar a prevenir la IHA

INTRODUCTION: Variceal upper gastrointestinal bleeding (UGIB) can trigger acute hypoxic hepatitis (AHH). The aim of this study was to analyse the incidence, associated risk factors and mortality of AHH after variceal UGIB. PATIENTS AND METHODS: Retrospective study of cirrhotic patients with variceal UGIB, classified into 2 groups according to the development of AHH. AHH was diagnosed when AST and ALT reached levels 10 times above the upper limit of normal, after ruling out other causes of hepatitis. The standard initial treatment consisted of haemodynamic support, emergency endoscopy with rubber band ligation, somatostatin and antibiotics. In the case of failure of primary haemostasis, a transjugular intrahepatic portosystemic shunt (TIPS) was implanted. Both groups (AHH and non-AHH) were compared. RESULTS: Sixty-eight cirrhotic patients with variceal UGIB admitted to the gastroenterology department of Hospital Ramón y Cajal between January 2007 and March 2012 were analysed. Eleven of these patients (16.2%) developed AHH. Univariate analysis showed the following items as risk factors: diabetes (OR: 7.5; CI: 1.9-29), shock (OR: 8.5; CI: 2.06-34) and persistent bleeding (OR: 9.0, CI: 1.6-49, P = .03). However, multivariate analysis confirmed only diabetes (OR: 8.61; CI: 1.4-52.5) and shock (OR: 7.58; CI: 1.26-45.51) as risk factors. Mortality rate in the AHH group was 45%, compared to 10.5% in the non-HAA group (P = .012). CONCLUSIONS: AHH after variceal UGIB occurred in 16.2% of cirrhotic patients and was associated with a poorer prognosis, with a mortality rate of 45%. Our findings suggest that diabetes and shock are risk factors for the development of AHH. Early identification of at-risk patients could therefore help prevent AHH

[Acute liver ischaemia after gastro-oesophageal variceal bleeding]. / Isquemia hepática aguda tras hemorragia digestiva alta por varices esofagogástricas.

INTRODUCTION: Variceal upper gastrointestinal bleeding (UGIB) can trigger acute hypoxic hepatitis (AHH). The aim of this study was to analyse the incidence, associated risk factors and mortality of AHH after variceal UGIB. PATIENTS AND METHODS: Retrospective study of cirrhotic patients with variceal UGIB, classified into 2 groups according to the development of AHH. AHH was diagnosed when AST and ALT reached levels 10 times above the upper limit of normal, after ruling out other causes of hepatitis. The standard initial treatment consisted of haemodynamic support, emergency endoscopy with rubber band ligation, somatostatin and antibiotics. In the case of failure of primary haemostasis, a transjugular intrahepatic portosystemic shunt (TIPS) was implanted. Both groups (AHH and non-AHH) were compared. RESULTS: Sixty-eight cirrhotic patients with variceal UGIB admitted to the gastroenterology department of Hospital Ramón y Cajal between January 2007 and March 2012 were analysed. Eleven of these patients (16.2%) developed AHH. Univariate analysis showed the following items as risk factors: diabetes (OR: 7.5; CI: 1.9-29), shock (OR: 8.5; CI: 2.06-34) and persistent bleeding (OR: 9.0, CI: 1.6-49, P=.03). However, multivariate analysis confirmed only diabetes (OR: 8.61; CI: 1.4-52.5) and shock (OR: 7.58; CI: 1.26-45.51) as risk factors. Mortality rate in the AHH group was 45%, compared to 10.5% in the non-HAA group (P=.012). CONCLUSIONS: AHH after variceal UGIB occurred in 16.2% of cirrhotic patients and was associated with a poorer prognosis, with a mortality rate of 45%. Our findings suggest that diabetes and shock are risk factors for the development of AHH. Early identification of at-risk patients could therefore help prevent AHH.

Orbital metastasis from hepatocellular carcinoma

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Pancreatitis aguda por hipertrigliceridemia / Acute hypertrygliceridemic pancreatitis

La pancreatitis aguda por hipertrigliceridemia es la tercera causa de pancreatitis aguda en la población occidental. Normalmente hay una alteración subyacente del metabolismo lipidémico, sobre la que actúa un factor secundario. La presentación clínica es similar a la de las pancreatitis agudas de otras etiologías, aunque su curso parece ser más tórpido y recurrente. Para su diagnóstico hay que saber que algunos parámetros de la analítica pueden estar artefactados, lo que puede conducir a un fallo en el diagnóstico. Tal es el caso de la amilasa, que puede estar falsamente descendida. El tratamiento se basa en sueroterapia intensa y analgesia. Cuando no responde al tratamiento conservador, deben utilizarse otros métodos para disminuir el nivel de triglicéridos. Para ello disponemos de la plasmaféresis, la insulina y la heparina. Este artículo pretende mostrar una revisión de la literatura actual sobre esta patología (AU)

Acute hypertriglyceridemic pancreatitis is the third cause of acute pancreatitis in the Western population. There is usually an underlying alteration in lipid metabolism and a secondary factor. Clinical presentation is similar to that of pancreatitis of other etiologies, but the course of acute hypertriglyceridemic pancreatitis seems to be worse and more recurrent. Some laboratory data can be artefacts, leading to diagnostic errors. This is the case of amylase, which can show false low levels. Treatment is based on intense fluidotherapy and analgesia. When there is no response to conservative management, other methods to lower triglyceride levels should be used. Several options are available, such as plasmapheresis, insulin, and heparin. The present article provides a review of the current literature on this entity (AU)

[Acute hypertrygliceridemic pancreatitis]. / Pancreatitis aguda por hipertrigliceridemia.

Acute hypertriglyceridemic pancreatitis is the third cause of acute pancreatitis in the Western population. There is usually an underlying alteration in lipid metabolism and a secondary factor. Clinical presentation is similar to that of pancreatitis of other etiologies, but the course of acute hypertriglyceridemic pancreatitis seems to be worse and more recurrent. Some laboratory data can be artefacts, leading to diagnostic errors. This is the case of amylase, which can show false low levels. Treatment is based on intense fluidotherapy and analgesia. When there is no response to conservative management, other methods to lower triglyceride levels should be used. Several options are available, such as plasmapheresis, insulin, and heparin. The present article provides a review of the current literature on this entity.