RESUMO
ABSTRACT Background. In clinical practice, it is assumed that a severe rise in transaminases is caused by ischemic, viral or toxic hepatitis. Nevertheless, cases of biliary obstruction have increasingly been associated with significant hypertransaminemia. With this study, we sought to determine the true etiology of marked rise in transaminases levels, in the context of an emergency department. Material and methods. We retrospectively identified all patients admitted to the emergency unit at Centro Hospitalar e Universitário de Coimbra between 1st January 2010 and 31st December 2010, displaying an increase of at least one of the transaminases by more than 15 times. All patient records were analyzed in order to determine the cause of hypertransaminemia. Results. We analyzed 273 patients - 146 males, mean age 65.1 ± 19.4 years. The most frequently etiology found for marked hypertransaminemia was pancreaticobiliary acute disease (n = 142;39.4%), mostly lithiasic (n = 113;79.6%), followed by malignancy (n = 74;20.6%), ischemic hepatitis (n = 61;17.0%), acute primary hepatocellular disease (n = 50;13.9%) and muscle damage (n = 23;6.4%). We were not able to determine a diagnosis for 10 cases. There were 27 cases of recurrence in the lithiasic pancreaticobiliary pathology group. Recurrence was more frequent in the group of patients who had not been submitted to early cholecystectomy after the first episode of biliary obstruction (p = 0.014). The etiology of hypertransaminemia varied according to age, cholestasis and glutamic-pyruvic transaminase values. Conclusion. Pancreaticobiliary lithiasis is the main cause of marked hypertransaminemia. Hence, it must be considered when dealing with such situations. Not performing cholecystectomy early on, after the first episode of biliary obstruction, may lead to recurrence.
Assuntos
Humanos , Pessoa de Meia-Idade , Idoso , Idoso de 80 Anos ou mais , Aspartato Aminotransferases/sangue , Biomarcadores/sangue , Cálculos Biliares/sangue , Alanina Transaminase/sangue , Admissão do Paciente , Portugal , Recidiva , Colecistectomia , Cálculos Biliares/cirurgia , Cálculos Biliares/diagnóstico , Cálculos Biliares/etiologia , Regulação para Cima , Valor Preditivo dos Testes , Estudos Retrospectivos , Fatores de Risco , Serviço Hospitalar de EmergênciaRESUMO
BACKGROUND: In clinical practice, it is assumed that a severe rise in transaminases is caused by ischemic, viral or toxic hepatitis. Nevertheless, cases of biliary obstruction have increasingly been associated with significant hypertransaminemia. With this study, we sought to determine the true etiology of marked rise in transaminases levels, in the context of an emergency department. MATERIAL AND METHODS: We retrospectively identified all patients admitted to the emergency unit at Centro Hospitalar e Universitário de Coimbra between 1st January 2010 and 31st December 2010, displaying an increase of at least one of the transaminases by more than 15 times. All patient records were analyzed in order to determine the cause of hypertransaminemia. RESULTS: We analyzed 273 patients - 146 males, mean age 65.1 ± 19.4 years. The most frequently etiology found for marked hypertransaminemia was pancreaticobiliary acute disease (n = 142;39.4%), mostly lithiasic (n = 113;79.6%), followed by malignancy (n = 74;20.6%), ischemic hepatitis (n = 61;17.0%), acute primary hepatocellular disease (n = 50;13.9%) and muscle damage (n = 23;6.4%). We were not able to determine a diagnosis for 10 cases. There were 27 cases of recurrence in the lithiasic pancreaticobiliary pathology group. Recurrence was more frequent in the group of patients who had not been submitted to early cholecystectomy after the first episode of biliary obstruction (p = 0.014). The etiology of hypertransaminemia varied according to age, cholestasis and glutamic-pyruvic transaminase values. CONCLUSION: Pancreaticobiliary lithiasis is the main cause of marked hypertransaminemia. Hence, it must be considered when dealing with such situations. Not performing cholecystectomy early on, after the first episode of biliary obstruction, may lead to recurrence.
Assuntos
Alanina Transaminase/sangue , Aspartato Aminotransferases/sangue , Cálculos Biliares/sangue , Idoso , Idoso de 80 Anos ou mais , Biomarcadores/sangue , Colecistectomia , Serviço Hospitalar de Emergência , Feminino , Cálculos Biliares/diagnóstico , Cálculos Biliares/etiologia , Cálculos Biliares/cirurgia , Humanos , Masculino , Pessoa de Meia-Idade , Admissão do Paciente , Portugal , Valor Preditivo dos Testes , Recidiva , Estudos Retrospectivos , Fatores de Risco , Regulação para CimaRESUMO
La hepatitis isquémica o hipóxica es una entidad clínica caracterizada por una importante elevación de las amino-transferasas de forma aguda y reversible que ocurre en aquellas situaciones que pueden ocasionar una reducción del flujo sanguíneo hepático, especialmente la insuficiencia cardiaca; sin embargo, se trata de un diagnóstico de exclusión ya que se deben descartar previamente otras causas potencialmente responsables de una hepatitis aguda, especialmente víricas y farmacológicas. Histológicamente se caracteriza por una necrosis centrolobulillar. Se presenta un caso ingresado en el servicio de medicina interna durante un periodo de dos meses
Ischemic hepatitis is characterized by a marked and reversible elevation in either the serum alanine or aspartate aminotransferase level in a appropriate clinical setting that could lead to a reduction in hepatic blood flow, mainly in patients with heart failure. To establish the diagnosis other causes of hepatitis, such as virus and drugs, must be previously excluded. Centrilobular necrosis is the main histologic feature. In the present study we describe the one cases of ischemic hepatitis seen in our medical service during a period of two months.
Assuntos
Humanos , Hepatite , Velocidade do Fluxo Sanguíneo , Cardiopatias Congênitas , FígadoRESUMO
A medida que la insuficiencia cardíaca (IC) progresa hacia una fase avanzada, otros sistemas también se deterioran, debido a un aumento en la incapacidad de responder a los requerimientos metabólicos de órganos principales y de músculos esqueléticos. Mientras que mucha atención se ha puesto en el estudio de la relación entre la IC y la falla renal, ha sido poco descrito el impacto de la IC avanzada y la disfunción hepática, siendo ésta una manifestación de comorbilidad, fundamentalmente, en los pacientes que se reinternan descompensados. La presencia de estos síntomas puede desviar tempranamente el diagnóstico, en lugar de considerar la patología cardíaca primaria, llevando a una demora en el inicio de intervenciones terapéuticas que mejoren el pronóstico y la sobrevida. En esta actualización, se realiza una revisión de la información contemporánea sobre los hallazgos histopatológicos, bioquímicos y clínicos de las entidades agudas y crónicas que conforman el síndrome cardio-hepático, así como su implicancia pronóstica, con el objetivo de establecer herramientas claras para el diagnóstico temprano y certero de esta entidad. Finalmente, se discuten las estrategias potenciales para investigar, manejar y tratar las interacciones cardio-hepáticas en los pacientes con IC avanzada.(AU)
As heart failure (HF) progresses toward the advanced stage, other systems also deteriorate due to an increase in the inability to respond to the metabolic requirements of organs and skeletal muscle. While much attention has focused on the study of the relationship between HF and renal failure, it has been poorly described the impact of advanced HF and liver dysfunction, this being a manifestation of comorbidity, mainly in patients who where admitted for decompensated HF. The presence of these symptoms can divert early diagnosis, instead of considering the primary cardiac pathology, leading to a delay in the onset of therapeutic interventions that improve the prognosis and survival. In this update, a review of contemporary information on histopathological, biochemical and clinical findings of acute and chronic conditions that make the cardiohepatic syndrome and its prognostic implication is performed, in order to establish clear diagnostic tools early and accurate of this entity. Finally, potential strategies to investigate, manage and treat cardiohepatic interactions in patients with advanced HF are discussed.(AU)
Conforme a insuficiÛncia cardíaca (IC) progride para a fase avanþada, outros sistemas também deteriorarem-se devido a um aumento na incapacidade de responder aos requerimentos metabólicos dos órgÒos e dos músculos esqueléticos. Embora muita atenþÒo tem focado sobre o estudo da relaþÒo entre a IC e insuficiÛncia renal, tem sido pouco descrito o impacto da IC avanþada e disfunþÒo hepática, sendo esta uma manifestaþÒo de comorbidades, principalmente pacientes admitidos por IC descompensada. A presenþa destes sintomas pode desviar o diagnóstico precoce, em vez de considerar a patologia cardíaca primária, que conduz a um atraso no aparecimento das intervenþ§es terapÛuticas que melhoram o prognóstico e sobrevivÛncia. Nesta atualizaþÒo foi realizada uma revisÒo de informaþ§es contemporÔneas sobre observaþ§es histopatológicas, bioquímicos e clínicos de doenþas agudas e cr¶nicas que fazem a síndrome cardio-hepática e suas implicaþ§es de prognóstico, com o objetivo de estabelecer ferramentas claras para o diagnóstico precoce e preciso desta entidade. Finalmente, analisam-se as estratégias potenciais para investigar, controlar e tratar as interaþ§es cardio-hepática em pacientes com IC avanþada.(AU)
RESUMO
A medida que la insuficiencia cardíaca (IC) progresa hacia una fase avanzada, otros sistemas también se deterioran, debido a un aumento en la incapacidad de responder a los requerimientos metabólicos de órganos principales y de músculos esqueléticos. Mientras que mucha atención se ha puesto en el estudio de la relación entre la IC y la falla renal, ha sido poco descrito el impacto de la IC avanzada y la disfunción hepática, siendo ésta una manifestación de comorbilidad, fundamentalmente, en los pacientes que se reinternan descompensados. La presencia de estos síntomas puede desviar tempranamente el diagnóstico, en lugar de considerar la patología cardíaca primaria, llevando a una demora en el inicio de intervenciones terapéuticas que mejoren el pronóstico y la sobrevida. En esta actualización, se realiza una revisión de la información contemporánea sobre los hallazgos histopatológicos, bioquímicos y clínicos de las entidades agudas y crónicas que conforman el síndrome cardio-hepático, así como su implicancia pronóstica, con el objetivo de establecer herramientas claras para el diagnóstico temprano y certero de esta entidad. Finalmente, se discuten las estrategias potenciales para investigar, manejar y tratar las interacciones cardio-hepáticas en los pacientes con IC avanzada.
As heart failure (HF) progresses toward the advanced stage, other systems also deteriorate due to an increase in the inability to respond to the metabolic requirements of organs and skeletal muscle. While much attention has focused on the study of the relationship between HF and renal failure, it has been poorly described the impact of advanced HF and liver dysfunction, this being a manifestation of comorbidity, mainly in patients who where admitted for decompensated HF. The presence of these symptoms can divert early diagnosis, instead of considering the primary cardiac pathology, leading to a delay in the onset of therapeutic interventions that improve the prognosis and survival. In this update, a review of contemporary information on histopathological, biochemical and clinical findings of acute and chronic conditions that make the cardiohepatic syndrome and its prognostic implication is performed, in order to establish clear diagnostic tools early and accurate of this entity. Finally, potential strategies to investigate, manage and treat cardiohepatic interactions in patients with advanced HF are discussed.
Conforme a insuficiência cardíaca (IC) progride para a fase avançada, outros sistemas também deteriorarem-se devido a um aumento na incapacidade de responder aos requerimentos metabólicos dos órgãos e dos músculos esqueléticos. Embora muita atenção tem focado sobre o estudo da relação entre a IC e insuficiência renal, tem sido pouco descrito o impacto da IC avançada e disfunção hepática, sendo esta uma manifestação de comorbidades, principalmente pacientes admitidos por IC descompensada. A presença destes sintomas pode desviar o diagnóstico precoce, em vez de considerar a patologia cardíaca primária, que conduz a um atraso no aparecimento das intervenções terapêuticas que melhoram o prognóstico e sobrevivência. Nesta atualização foi realizada uma revisão de informações contemporâneas sobre observações histopatológicas, bioquímicos e clínicos de doenças agudas e crônicas que fazem a síndrome cardio-hepática e suas implicações de prognóstico, com o objetivo de estabelecer ferramentas claras para o diagnóstico precoce e preciso desta entidade. Finalmente, analisam-se as estratégias potenciais para investigar, controlar e tratar as interações cardio-hepática em pacientes com IC avançada.
Assuntos
Humanos , Insuficiência Cardíaca , Hepatite , HepatopatiasRESUMO
Hypoxic hepatitis (HH), or ischemic hepatitis occurs in the context of cardiac, circulatory or respiratory failure and is characterized by a sharp increase in serum aminotransferase levels due to anoxic necrosis of centrilobular liver cells. It is frequently observed in the ICU and has been associated to increased patient morbidity and mortality. Hepatic ischemia in the presence of a shock state is the main hemodynamic mechanism. However, other hemodynamic mechanisms of hypoxia, such as hepatic passive congestion, arterial hypoxemia and tissue dysoxia play an important role. Shock state is observed in only 50 percent of the cases. HH therapy of depends primarily on the nature of the underlying condition. Patients with HH have poor prognosis with more than 50 percent of mortality during the hospital stay.
Hepatitis hipóxica (HH) o hepatitis isquémica se presenta en el contexto de insuficiencia cardíaca, respiratoria o circulatoria y se caracteriza por aumento brusco de transaminasas debido a la necrosis por anoxia de las células centrilobulillares del hígado. La HH es frecuente en UCI y está asociada a un aumento en la morbilidad y mortalidad. La isquemia hepática por un estado de shock es la principal causa. Sin embargo, mecanismos de hipoxia como la congestión pasiva del hígado, hipoxemia arterial y disoxia tisular juegan un importante rol. Se shock observa en sólo 50 por ciento de los casos. El tratamiento depende primariamente de la causa subyacente. Los pacientes con HH tienen un mal pronóstico con más de 50 por ciento de mortalidad intrahospitalaria.
Assuntos
Humanos , Hipóxia/complicações , Hipóxia/terapia , Hepatite/complicações , Hepatite/terapia , Choque , Hipóxia/mortalidade , Hepatite/mortalidade , Isquemia , PrognósticoRESUMO
Transjugular intrahepatic portosystemic shunt (TIPS) is a safe and effective procedure for the treatment of complications of liver cirrhosis, such as refractory ascites, hepatic hydrothorax and refractory variceal bleeding. The aim of this paper is to describe a rare case of liver failure after a TIPS procedure. A 38-year-old diabetic male with Child-Pugh C liver cirrhosis due to chronic hepatitis C infection who had developed refractory ascites was scheduled for a TIPS procedure. Within 24 h following TIPS placement, the patient developed distributive shock, jaundice, persistentgrade 3 hepatic encephalopathy, severe coagulopathy and acute renal failure. He was treated with lactulose enemas, broad-spectrum antibiotics and blood-derived products. Laboratory data revealed a 100-fold increase in aminotransferases and a non-enhanced computed tomography showed an irregular hypodense area in the right posterior segment of the liver. Despite being initially being in a stable condition, the patient developed progressive liver failure and died 2 mo later. Hepatic infarction is an uncommon phenomenon after a TIPS procedure; however, it can greatly complicate the course of a disease in a patient with an already compromised liver function.