RESUMO
Hypoxic hepatitis is an uncommon cause of hepatic damage characterized by a centrolobular necrosis. Its pathophysiology remains unclear. Aortic dissection is a rare but frequently catastrophic event. It is caused by an aortic intimal tear with propagation of a false channel in the media. Depending on the site and extension, it can cause hypoperfusion of any organ leading to cellular ischemia and necrosis. We are presenting a case of hypoxic hepatitis in a patient with an extensive aortic dissection who present to the emergency department.
Assuntos
Dissecção Aórtica/complicações , Hepatite/etiologia , Isquemia/etiologia , Fígado/irrigação sanguínea , Dor Abdominal/etiologia , Dissecção Aórtica/diagnóstico , Dissecção Aórtica/fisiopatologia , Aneurisma Aórtico/complicações , Aneurisma Aórtico/diagnóstico por imagem , Dispneia/etiologia , Emergências , Evolução Fatal , Hepatite/diagnóstico por imagem , Humanos , Masculino , Pessoa de Meia-Idade , Tomografia Computadorizada por Raios XRESUMO
Hypoxic hepatitis is an uncommon cause of hepatic damage characterized by a centrolobular necrosis. Its pathophysiology remains unclear. Aortic dissection is a rare but frequently catastrophic event. It is caused by an aortic intimal tear with propagation of a false channel in the media. Depending on the site and extension, it can cause hypoperfusion of any organ leading to cellular ischemia and necrosis. We are presenting a case of hypoxic hepatitis in a patient with an extensive aortic dissection who present to the emergency department.
La hepatitis hipóxica es una causa poco frecuente de daño hepático caracterizada por una necrosis centrolobular. Su fisiopatología sigue siendo poco clara. La disección aórtica es un evento raro pero con frecuencia catastrófico. Dependiendo del sitio y la extensión, puede causar hipoperfusión de cualquier órgano lo que conduce a una isquemia celular y necrosis. Nosotros presentamos un caso de hepatitis hipóxica en un paciente con disección aórtica extensa que se presenta al servicio de emergencia.
Assuntos
Humanos , Masculino , Pessoa de Meia-Idade , Hepatite/etiologia , Isquemia/etiologia , Dissecção Aórtica/complicações , Fígado/irrigação sanguínea , Aneurisma Aórtico/complicações , Aneurisma Aórtico/diagnóstico por imagem , Tomografia Computadorizada por Raios X , Dor Abdominal/etiologia , Evolução Fatal , Dispneia/etiologia , Emergências , Hepatite/diagnóstico por imagem , Dissecção Aórtica/diagnóstico , Dissecção Aórtica/fisiopatologiaRESUMO
Gastroesophageal junction adenocarcinoma on esophagogastroduodenoscopy biopsy. Initial PET-CT showed no definite evidence of distant metastatic disease. One month after radiation treatment, repeat PET-CT showed interval decrease in size of gastroesophageal mass but new multifocal FDG avidity in the caudate and left hepatic lobes. Correlation with contrast-enhanced CT and US images was negative, making metastasis less likely. Ultrasound-guided biopsy confirmed radiation-induced hepatitis, which caused false positively increased FDG uptake from inflammatory changes.
Assuntos
Adenocarcinoma/radioterapia , Neoplasias Esofágicas/radioterapia , Hepatite/diagnóstico por imagem , Lesões por Radiação/diagnóstico por imagem , Radioterapia Conformacional/efeitos adversos , Neoplasias Gástricas/radioterapia , Adenocarcinoma/diagnóstico por imagem , Adenocarcinoma/patologia , Diagnóstico Diferencial , Neoplasias Esofágicas/diagnóstico por imagem , Neoplasias Esofágicas/patologia , Junção Esofagogástrica/diagnóstico por imagem , Junção Esofagogástrica/patologia , Fluordesoxiglucose F18 , Hepatite/etiologia , Hepatite/patologia , Humanos , Biópsia Guiada por Imagem , Tomografia por Emissão de Pósitrons combinada à Tomografia Computadorizada , Lesões por Radiação/etiologia , Lesões por Radiação/patologia , Compostos Radiofarmacêuticos , Neoplasias Gástricas/diagnóstico por imagem , Neoplasias Gástricas/patologia , Tomografia Computadorizada por Raios X , UltrassonografiaAssuntos
Fluordesoxiglucose F18/administração & dosagem , Granuloma/diagnóstico , Hepatite/diagnóstico , Neoplasias Hepáticas/diagnóstico , Imagem Multimodal/métodos , Tomografia por Emissão de Pósitrons , Compostos Radiofarmacêuticos/administração & dosagem , Tomografia Computadorizada por Raios X , Anti-Inflamatórios/uso terapêutico , Biópsia , Colchicina/uso terapêutico , Diagnóstico Diferencial , Feminino , Granuloma/diagnóstico por imagem , Granuloma/tratamento farmacológico , Hepatite/diagnóstico por imagem , Hepatite/tratamento farmacológico , Humanos , Testes de Função Hepática , Neoplasias Hepáticas/diagnóstico por imagem , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Resultado do TratamentoRESUMO
BACKGROUND: At the present time, there is no accepted treatment for non-alcoholic steatohepatitis (NASH); nevertheles, there are some reports of non-controlled studies with apparently good answer with ursodeoxycholic acid (UDCA) as much with alpha-tocopherol (aTP). OBJECTIVE: To value the clinical, biochemical and hepatic ultrasound (US) response in patients with NASH in treatment for 1 year with UDCA or aTP, as well as to establish tolerance, undesirable effects and fulfillment. METHOD: Three patients received UDCA (250 mg TID) and six aTP (100 mg TID). Changes in hepatic function test and US were analyzed. All patients were women with an average age of 52 years, body mass index of 27, five with diabetes mellitus (DM) type II. RESULTS: Fulfillment of treatment was 95%; undesirable effects were not reported; clinical course was asymptomatic and clinically we did not observe important changes; US showed favorable changes in four patients (44%), two in each group. Alkaline phosphatase was normalized in patient who initially registered it as high. ALT and AST average diminished by 40% and normalization was obtained in five of six patients in treatment with aTP (83%) and in one of the UDCA group (33%). No statistically significant difference was obtained. CONCLUSIONS: The group is small and requires more persons and to be compared with a control group. It is possible that both drugs can be useful in the treatment of NASH; they are well tolerated and allow good fulfillment.
Assuntos
Antioxidantes/uso terapêutico , Colagogos e Coleréticos/uso terapêutico , Fígado Gorduroso/tratamento farmacológico , Hepatite/tratamento farmacológico , Ácido Ursodesoxicólico/uso terapêutico , alfa-Tocoferol/uso terapêutico , Adulto , Idoso , Fosfatase Alcalina/sangue , Antioxidantes/administração & dosagem , Colagogos e Coleréticos/administração & dosagem , Ensaios Enzimáticos Clínicos , Interpretação Estatística de Dados , Fígado Gorduroso/diagnóstico , Fígado Gorduroso/diagnóstico por imagem , Feminino , Seguimentos , Hepatite/diagnóstico , Hepatite/diagnóstico por imagem , Humanos , Pessoa de Meia-Idade , Fatores de Tempo , Transaminases/sangue , Ultrassonografia , Ácido Ursodesoxicólico/administração & dosagem , alfa-Tocoferol/administração & dosagemRESUMO
BACKGROUND: The normal length of the pancreaticobiliary union (common channel) in the pediatric population is not known, nor is the frequency of anomalous pancreaticobiliary union and the extent to which it is associated with pancreaticobiliary disease. METHODS: ERCP was performed on 136 patients younger than 1 year (group 1) and 128 older than 1 year (group 2). RESULTS: In group 1 the average length of the common channel was 1.8 +/- 0.61 mm with a maximal length of 3 mm (mean plus 2 standard deviations). In group 2 the average length and maximal length of the common channel increased with age. In the 1 to 3 year age range the average length was 2.2 +/- 0.47 mm with a maximal length of 2.7 mm, in the 4 to 6 year range it was 2.8 +/- 0.40 mm (3.6 mm maximal), in the 7 to 9 year range it was 3.2 +/- 0.43 mm (4.1 mm maximal), in the 10 to 12 year range it was 3.9 +/- 0.5 mm (4.4 mm maximal), and in the 13 to 15 year range it was 4.0 +/- 0.51 mm (5 mm maximal). The prevalence of the anomalous pancreaticobiliary union was 25% (66/264). In group 1 the anomaly was present in 4.4% (6 of 136) of patients, 1.3% (1/76) with neonatal hepatitis, 4.6% (3/44) with biliary atresia, and 100% (2/2) with choledochal cyst. In group 2 the anomaly was present in 46.9% (60/128) of patients, 100% (57/57) with choledochal cyst and 15.7% (3/19) with idiopathic recurrent pancreatitis without bile duct dilatation. CONCLUSIONS: The mean length of the common channel increases with age. The maximum normal length of the common channel in neonates and infants younger than 1 year is 3 mm. It increases with age to a maximum of 5 mm in children and adolescents between 13 and 15 years of age. Anomalous pancreaticobiliary union is relatively common among children and adolescents undergoing ERCP in our center, including those with idiopathic recurrent pancreatitis (15.7%). ERCP is valuable in the diagnosis of this anomaly.
Assuntos
Colangiopancreatografia Retrógrada Endoscópica , Ducto Colédoco/anormalidades , Ductos Pancreáticos/anormalidades , Adolescente , Atresia Biliar/diagnóstico por imagem , Criança , Pré-Escolar , Cisto do Colédoco/diagnóstico por imagem , Doença Crônica , Ducto Colédoco/diagnóstico por imagem , Feminino , Hepatite/diagnóstico por imagem , Humanos , Lactente , Recém-Nascido , Masculino , Ductos Pancreáticos/diagnóstico por imagem , Pancreatite/diagnóstico por imagem , Valores de ReferênciaRESUMO
We retrospectively evaluated the utility of hepatobiliary scintigraphy and various clinical factors in differentiating intrahepatic cholestasis from biliary atresia in 28 consecutive infants with neonatal cholestasis. One millicurie of technetium-labeled diisopropyliminodiacetic acid (DISIDA) was administered intravenously, and images were obtained for up to 24 hours or until gastrointestinal excretion was noted. Nine separate studies in seven infants with biliary atresia were correctly interpreted as showing no gastrointestinal excretion of radionuclide. Of the 21 patients with intrahepatic cholestasis, only nine had gastrointestinal excretion on the first study; in eight without excretion, a second study was done, and five of these showed gut excretion. All infants with either neonatal hepatitis (six) or inspissated bile syndrome (three) had demonstrable gastrointestinal excretion either on the first or second DISIDA study. However, five of six infants with paucity of intrahepatic bile ducts, two of six infants with cholestasis secondary to total parenteral nutrition, and one infant with cholangiolitis did not show evidence of gastrointestinal excretion. The mean birth weight, mean gestational age, and mean weight at study were significantly greater (P less than 0.005) for infants with biliary atresia without excretion than for infants with intrahepatic cholestasis without excretion. The mean direct bilirubin concentration was 6.0 mg/dL for both infants with biliary atresia and infants with intrahepatic cholestasis without excretion; however, infants with excretion had a significantly lower (P less than 0.02) mean direct bilirubin value of 3.4 mg/dL. Excretion was noted in four infants with total bilirubin values greater than 10.0 mg/dL. The absence of gut excretion on the first DISIDA study was 100% sensitive but only 43% specific for biliary atresia. In infants without gut excretion of DISIDA, birth weight greater than 2200 g was 100% sensitive and 92% specific for biliary atresia. We conclude that DISIDA scanning, together with clinical data, is useful in differentiating extrahepatic from intrahepatic cholestasis. The absence of gut excretion on the first DISIDA study does not necessarily indicate extrahepatic obstruction; the study should be repeated if the diagnosis is not clear.