Mechanisms of the beneficial effect of sevoflurane in liver ischemia/reperfusion injury.

PURPOSE: To evaluate the underlying mechanisms by which sevoflurane protects the liver against ischemia/reperfusion injury evaluate the mechanism by which sevoflurane exerts this protective effect. METHODS: Twenty-six rats were subjected to partial ischemia/reperfusion injury for 1h: one group received no treatment, one group received sevoflurane, and sham group of animals received laparotomy only. Four hours after reperfusion, levels of alanine and aspartate aminotransferases, tumor necrosis factor-a, and interleukins 6 and 10 were measured. Analyses of mitochondrial oxidation and phosphorylation, malondialdehyde content, histology, and pulmonary vascular permeability were performed. RESULTS: Serum levels of alanine and aspartate aminotransferases were significantly lower in the sevoflurane group compared to untreated controls (p<0.05). The sevoflurane group also showed preservation of liver mitochondrial function compared to untreated controls (p<0.05). Sevoflurane administration did not alter increases in serum levels of tumor necrosis factor-a, and interleukins 6 and 10. Sevoflurane treatment significantly reduced the coagulative necrosis induced by ischemia/reperfusion (p<0.05). Pulmonary vascular permeability was preserved in the sevoflurane group compared to untreated controls. CONCLUSION: Sevoflurane administration protects the liver against ischemia/reperfusion injury, via preservation of mitochondrial function, and also preserves lung vascular permeability.

Mechanisms of the beneficial effect of sevoflurane in liver ischemia/reperfusion injury

PURPOSE: To evaluate the underlying mechanisms by which sevoflurane protects the liver against ischemia/reperfusion injury evaluate the mechanism by which sevoflurane exerts this protective effect. METHODS: Twenty-six rats were subjected to partial ischemia/reperfusion injury for 1h: one group received no treatment, one group received sevoflurane, and sham group of animals received laparotomy only. Four hours after reperfusion, levels of alanine and aspartate aminotransferases, tumor necrosis factor-a, and interleukins 6 and 10 were measured. Analyses of mitochondrial oxidation and phosphorylation, malondialdehyde content, histology, and pulmonary vascular permeability were performed. RESULTS: Serum levels of alanine and aspartate aminotransferases were significantly lower in the sevoflurane group compared to untreated controls (p<0.05). The sevoflurane group also showed preservation of liver mitochondrial function compared to untreated controls (p<0.05). Sevoflurane administration did not alter increases in serum levels of tumor necrosis factor-a, and interleukins 6 and 10. Sevoflurane treatment significantly reduced the coagulative necrosis induced by ischemia/reperfusion (p<0.05). Pulmonary vascular permeability was preserved in the sevoflurane group compared to untreated controls. CONCLUSION: Sevoflurane administration protects the liver against ischemia/reperfusion injury, via preservation of mitochondrial function, and also preserves lung vascular permeability.

Modelo experimental de choque hemorrágico não controlado em porcos / Experimental model of non-controlled hemorrhagic shock in pigs / Modelo experimental de choque hemorrágico no controlado en cerdos

JUSTIFICATIVA E OBJETIVOS: Uma compreensão melhor das alterações fisiopatológicas associadas ao trauma e ao choque hemorrágico pode ajudar no desenvolvimento de terapêuticas capazes de reduzir a mortalidade relacionada ao trauma. O objetivo deste estudo é descrever um modelo de choque hemorrágico não controlado em porcos. MÉTODOS: Como medicação pré-anestésica, os animais receberam cetamina e midazolan. A anestesia foi induzida com propofol e a intubação traqueal foi realizada na vigência de respiração espontânea. Após a intubação, realizou-se bloqueio neuromuscular. Os animais foram mantidos em respiração mecânica controlada e normocapnia. A anestesia foi mantida com propofol e fentanil, de acordo com a necessidade. Solução de soro fisiológico 0,9 por cento foi infundida em todo o período de preparação. MONITORAÇÃO: Foram utilizados cardioscópio, oxímetro de pulso, medida de pressão arterial invasiva, cateter volumétrico de artéria pulmonar e medida de débito urinário por cistostomia. Modelo experimental: após registro inicial de variáveis hemodinâmicas, metabólicas e de coagulação, realizaram-se incisão subcostal direita e biópsia hepática do lobo esquerdo. A infusão de anestésicos foi reduzida, enquanto a de solução de salina isotônica interrompida. Uma incisão de 12 cm de extensão por 2 cm de profundidade foi feita no lobo hepático direito, seguida de divulsão digital do ferimento. Durante a fase de hemorragia, uma sonda de aspiração foi posicionada junto ao ferimento e o volume de sangue aspirado foi registrado. Quando a pressão arterial média chegou a 40 mmHg e o sangramento foi superior a 700 mL, pôde ser iniciada a fase de intervenção de acordo com o tipo de estudo. CONCLUSÃO: É importante continuar o desenvolvimento de modelos experimentais com o objetivo final de reduzir a alta mortalidade e os custos associados ao trauma.

BACKGROUND AND OBJECTIVES: A better understanding of pathophysiologic changes associated to trauma and hemorrhagic shock can help the development of therapies capable of reducing trauma-related mortality. The objective of this study was to describe a model of non-controlled hemorrhagic shock in pigs. METHODS: Animals received ketamine and midazolam as pre-anesthetic medications. Anesthesia was induced with propofol, and tracheal intubation was performed with the animals on spontaneous ventilation. After intubation neuromuscular blockade was performed. Animals were maintained in controlled mechanical ventilation and normocapnia. Anesthesia was maintained with propofol and fentanyl as needed. Saline was infused during the entire preparation period. MONITORING: Cardioscope, pulse oximeter, invasive blood pressure, volumetric catheter in the pulmonary artery, and urine output by cystostomy were used. Experimental model: after the initial recording of hemodynamic, metabolic, and coagulation variables, right subcostal incision and left lobe liver biopsy were performed. Anesthetic infusion was reduced while the infusion of saline was interrupted. An incision 12 cm long 2 cm deep was performed in the right liver lobe followed by digital divulsion of the wound. During the hemorrhagic phase, an aspiration probe was placed close to the wound and the volume of aspirated blood was recorded. When mean arterial pressure reached 40 mmHg and bleeding was above 700 mL the intervention phase was initiated according to the type of study. CONCLUSION: The development of experimental models to reduce high mortality and costs related to trauma is important.

JUSTIFICATIVA Y OBJETIVOS: Una comprensión mejor de las alteraciones fisiopatológicas asociadas al trauma y al choque hemorrágico, puede ayudar en el desarrollo de las terapéuticas capaces de reducir la mortalidad relacionada con el trauma. El objetivo de este estudio es describir un modelo de choque hemorrágico no controlado en cerdos. MÉTODOS: Como medicación preanestésica, los animales recibieron cetamina y midazolan. La anestesia fue inducida con propofol, y la intubación traqueal fue realizada con la respiración espontánea. Después de la intubación, se realizó el bloqueo neuromuscular. Los animales se mantuvieron bajo respiración mecánica controlada y normocapnia. La anestesia se mantuvo con propofol y fentanil, a tono con la necesidad. Una solución de suero fisiológico al 0,9 por ciento fue infundida durante todo el período de la preparación. MONITOREO: Se usaron el cardioscopio, oxímetro de pulso, medida de presión arterial invasiva, catéter volumétrico de arteria pulmonar y medida de débito urinario por cistostomía. Modelo experimental: después del registro inicial de las variables hemodinámicas, metabólicas y de coagulación, se realizaron la incisión subcostal derecha y la biopsia hepática del lóbulo izquierdo. La infusión de anestésicos fue reducida, mientras que la solución de salina isotónica se interrumpió. Una incisión de 12 cm de extensión por 2 cm de profundidad se hizo en el lóbulo hepático derecho, seguida de una divulsión digital de la herida. Durante la fase de hemorragia, una sonda de aspiración fue posicionada junto a la herida, y el volumen de sangre aspirado fue registrado. Cuando la presión arterial promedio llegó a 40 mmHg y el sangramiento fue superior a 700 mL, pudo iniciarse la fase de intervención de acuerdo con el tipo de estudio. CONCLUSIÓN: Es importante continuar desarrollando modelos experimentales con el objetivo final de reducir la alta mortalidad y los costes asociados al trauma.

Experimental model of non-controlled hemorrhagic shock in pigs.

BACKGROUND AND OBJECTIVES: A better understanding of pathophysiologic changes associated to trauma and hemorrhagic shock can help the development of therapies capable of reducing trauma-related mortality. The objective of this study was to describe a model of non-controlled hemorrhagic shock in pigs. METHODS: Animals received ketamine and midazolam as pre-anesthetic medications. Anesthesia was induced with propofol, and tracheal intubation was performed with the animals on spontaneous ventilation. After intubation neuromuscular blockade was performed. Animals were maintained in controlled mechanical ventilation and normocapnia. Anesthesia was maintained with propofol and fentanyl as needed. Saline was infused during the entire preparation period. MONITORING: Cardioscope, pulse oximeter, invasive blood pressure, volumetric catheter in the pulmonary artery, and urine output by cystostomy were used. Experimental model: after the initial recording of hemodynamic, metabolic, and coagulation variables, right subcostal incision and left lobe liver biopsy were performed. Anesthetic infusion was reduced while the infusion of saline was interrupted. An incision 12cm long 2cm deep was performed in the right liver lobe followed by digital divulsion of the wound. During the hemorrhagic phase, an aspiration probe was placed close to the wound and the volume of aspirated blood was recorded. When mean arterial pressure reached 40mmHg and bleeding was above 700mL the intervention phase was initiated according to the type of study. CONCLUSION: The development of experimental models to reduce high mortality and costs related to trauma is important.

Liver transplantation for acute liver failure: a 5 years experience.

BACKGROUND: Fulminant hepatic failure carries a high morbidity and mortality. Liver transplantation has markedly improved the prognosis of patients with fulminant hepatic failure. AIM: To evaluate the outcome of 20 patients with acute liver failure and indication for liver transplantation. METHODS: A retrospective review of 20 patients with acute liver failure and indication for liver transplantation was performed. Patients were divided into two groups: group A with 12 patients who underwent liver transplantation and group B with 8 patients who did not receive liver transplantation. Both groups were analyzed according to age, sex, ABO blood type, etiology of acute liver failure, time on list until transplantation or death, and survival rates. Group A patients were additionally analyzed according to preoperative INR, AST, and ALT peak values and MELD (Model for End-stage Liver Disease) scores; intraoperative red blood cells and plasma transfusion and cold ischemia time; postoperative lenght of intensive care unit and hospital stay, and needed for dialysis. RESULTS: Group A: there were four men and eight women with an average age of 24.6 years. The average liver waiting time period was 3.4 days and MELD score 36. Seven patients are alive with good hepatic function at a medium follow-up of 26.2 months. The actuarial survival rate was 65.2% at 1 year. Group B: There were two men and six women with an average age of 30.9 years. The mean waiting time on list until death was 7.4 days. All patients died while waiting for a liver donor. CONCLUSION: Despite the improvements in intensive care management, most patients with acute liver failure and indication for liver transplantation ca not survive long without transplant. Liver transplantation is potentially the only curative modality and has markedly improved the prognosis of those patients.

Liver transplantation for acute liver failure: a 5 years experience / Transplante hepático na hepatite fulminante: uma experiência de 5 anos

BACKGROUND: Fulminant hepatic failure carries a high morbidity and mortality. Liver transplantation has markedly improved the prognosis of patients with fulminant hepatic failure. AIM: To evaluate the outcome of 20 patients with acute liver failure and indication for liver transplantation. METHODS: A retrospective review of 20 patients with acute liver failure and indication for liver transplantation was performed. Patients were divided into two groups: group A with 12 patients who underwent liver transplantation and group B with 8 patients who did not receive liver transplantation. Both groups were analyzed according to age, sex, ABO blood type, etiology of acute liver failure, time on list until transplantation or death, and survival rates. Group A patients were additionally analyzed according to preoperative INR, AST, and ALT peak values and MELD (Model for End-stage Liver Disease) scores; intraoperative red blood cells and plasma transfusion and cold ischemia time; postoperative lenght of intensive care unit and hospital stay, and needed for dialysis. RESULTS: Group A: there were four men and eight women with an average age of 24.6 years. The average liver waiting time period was 3.4 days and MELD score 36. Seven patients are alive with good hepatic function at a medium follow-up of 26.2 months. The actuarial survival rate was 65.2 percent at 1 year. Group B: There were two men and six women with an average age of 30.9 years. The mean waiting time on list until death was 7.4 days. All patients died while waiting for a liver donor. CONCLUSION: Despite the improvements in intensive care management, most patients with acute liver failure and indication for liver transplantation ca not survive long without transplant. Liver transplantation is potentially the only curative modality and has markedly improved the prognosis of those patients.

RACIONAL: OBJETIVO: Avaliar a evolução de 20 pacientes com insuficiência hepática aguda e indicação de transplante hepático. MÉTODOS: Foi realizado estudo retrospectivo de 20 pacientes com insuficiência hepática aguda e indicação de transplante hepático. Os pacientes foram divididos em dois grupos: grupo A com 12 pacientes que foram submetidos a transplante hepático e grupo B com oito pacientes não submetidos a transplante hepático. Ambos os grupos foram analisados de acordo com idade, sexo, tipagem sangüínea, etiologia da insuficiência hepática aguda, tempo em lista até o transplante ou até o óbito e sobrevida. Os pacientes do grupo A foram ainda analisados de acordo com o escore MELD (Model for End-stage Liver Disease), valores de pico pré-operatório de INR, AST e ALT, necessidade de transfusão de concentrado de hemácias e plasma fresco congelado durante o transplante, tempo de isquemia fria, tempo de permanência hospitalar e em unidade de terapia intensiva e necessidade de diálise no pós-transplante imediato. RESULTADOS: Grupo A: o tempo médio de espera em lista até o transplante foi de 3,4 dias e o MELD médio, de 36. Sete pacientes continuam vivos com boa função hepática em um tempo médio de seguimento de 26,2 meses. A sobrevida atuarial em 1 ano foi de 65,2 por cento. Grupo B: foram estudados dois homens e seis mulheres com média de idade de 30,9 anos. O tempo médio de espera em lista até o óbito foi de 7,4 dias. Todos os pacientes foram a óbito esperando por um doador. CONCLUSÃO: Mesmo com todos os avanços nos cuidados de terapia intensiva, a maioria dos pacientes com insuficiência hepática aguda e indicação de transplante hepático não sobrevivem por muito tempo sem o transplante. O transplante hepático é potencialmente a única terapêutica curativa atualmente disponível e melhorou consideravelmente o prognóstico desses pacientes.

Linfangioma cístico abdominal gigante em criança: relato de caso / Gigantic abdominal cystic lymphangioma in a child: a case report

Objetivo: Descrever o caso raro de uma criança do sexo masculino, de nove meses de idade, com linfangioma cístico abdominal gigante, e fazer breve revisão da literatura sobre o tema. Descrição: Lactente de nove meses, com aumento progressivo do volume abdominal havia três meses. Ao exame físico, havia sinais de anemia e presença de grande massa palpável no abdome. Ultra-sonografia abdominal evidenciou grande lesão cística com septações finas. O paciente foi tratado cirurgicamente, com boa evolução. Comentários: O linfangioma cístico abdominal é uma patologia rara na infância. Sua etiologia permanece desconhecida. O aumento do volume abdominal com presença de massa visível ou palpável ocorre em 25-73% dos casos. A resseção cirúrgica é o tratamento de escolha e o prognóstico é, em geral, bom...

Evolução inesperada em um paciente com cirrose hepática, ascite refratária e peritonite bacteriana espontânea de repetição / Unexpected evolution in a patient with liver cirrhosis, refractory acite, and repeated spontaneous bacterial peritonitis

Introdução: A combinação de cirrose hepática, ascite refratária e peritonite bacteriana espontânea (PBE) de repetição tem prognostico ruim e alta mortalidade. O transplante hepático é a única terapeutica atualmente disponível para esses pacientes. O objetivo é decrever uma evolução inesperada, com sobrevida em longo prazo sem transplante hepático, em um paciente com cirrose alcoólica, ascite refratária e PBE de repetição. Descrição: Paciente masculinoa, 44 anos, com cirrose alcoólica, ascite refratária e PEB de repetição. Apresentava MELD 22 e CHILD c12. Nos 18 mese anteriores, havia sido internado 10 vezes devido principalmente a PBE e encefalopatia e havia realizado 56 paracenteses de alívio. Após um mês em lista de espera, o paciente foi admitdio para transplante. Entretanto, durante o procedimento não foi possível abordar a topografia hepatica, devido a multiplas aderências ao redor do fígado. Diante da impossibilidade técnica realizou-se apenas limpeza ampla da cavidade abdominal. Inesperadamente, mais de 50 meses após a tentativa do transplante, o paciente continua vivo, com MELD 17 e CHILD B8 atuais. Discussão: O transplante hepático talvez seja a única terapêutica curativa atualmente disponível em pacientes com cirrose avançada, PBE de repetição e ascite refratária. Contudo, este relato mostra uma evolução inesperada em um paciente com essas co-morbidades que, mesmo sem transplante, evolui bem, com sobreida em longo prazo.