RESUMEN
INTRODUCTION AND OBJECTIVES: Acute liver failure, also known as fulminant hepatic failure (FHF), includes a spectrum of clinical entities characterized by acute liver injury, severe hepatocellular dysfunction and hepatic encephalopathy. The objective of this study was to assess cerebral autoregulation (CA) in 25 patients (19 female) with FHF and to follow up with seventeen of these patients before and after liver transplantation. PATIENTS AND METHODS: The mean age was 33.8 years (range 14-56, SD 13.1 years). Cerebral hemodynamics was assessed by transcranial Doppler (TCD) bilateral recordings of cerebral blood velocity (CBv) in the middle cerebral arteries (MCA). RESULTS: CA was assessed based on the static CA index (SCAI), reflecting the effects of a 20-30 mmHg increase in mean arterial blood pressure on CBv induced with norepinephrine infusion. SCAI was estimated at four time points: pretransplant and on the 1st, 2nd and 3rd posttransplant days, showing a significant difference between pre- and posttransplant SCAI (p = 0.005). SCAI peaked on the third posttransplant day (p = 0.006). Categorical analysis of SCAI showed that for most patients, CA was reestablished on the second day posttransplant (SCAI > 0.6). CONCLUSIONS: These results suggest that CA impairment pretransplant and on the 1st day posttransplant was re-established at 48-72 h after transplantation. These findings can help to improve the management of this patient group during these specific phases, thereby avoiding neurological complications, such as brain swelling and intracranial hypertension.
Asunto(s)
Encefalopatía Hepática , Fallo Hepático Agudo , Trasplante de Hígado , Humanos , Femenino , Adolescente , Adulto Joven , Adulto , Persona de Mediana Edad , Trasplante de Hígado/efectos adversos , Encefalopatía Hepática/diagnóstico por imagen , Encefalopatía Hepática/etiología , Fallo Hepático Agudo/diagnóstico , Fallo Hepático Agudo/cirugía , Fallo Hepático Agudo/complicaciones , Homeostasis/fisiologíaRESUMEN
Disorders of the mesenteric, portal, and hepatic veins and mesenteric and hepatic arteries have important clinical consequences and may lead to acute liver failure, chronic liver disease, noncirrhotic portal hypertension, cirrhosis, and hepatocellular carcinoma. Although literature in the field of vascular liver disorders is scant, these disorders are common in clinical practice, and general practitioners, gastroenterologists, and hepatologists may benefit from expert guidance and recommendations for management of these conditions. These guidelines represent the official practice recommendations of the American College of Gastroenterology. Key concept statements based on author expert opinion and review of literature and specific recommendations based on PICO/GRADE analysis have been developed to aid in the management of vascular liver disorders. These recommendations and guidelines should be tailored to individual patients and circumstances in routine clinical practice.
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Humanos , Circulación Esplácnica/fisiología , Manejo de Atención al Paciente/organización & administración , Fallo Hepático Agudo/complicaciones , Circulación HepáticaRESUMEN
Acute liver failure (ALF) is a severe condition secondary to a myriad of causes associated with poor outcomes. The prompt diagnosis and identification of the aetiology allow the administration of specific treatments plus supportive strategies and to define the overall prognosis, the probability of developing complications and the need for liver transplantation. Pivotal issues are adequate monitoring and the institution of prophylactic strategies to reduce the risk of complications, such as progressive liver failure, cerebral oedema, renal failure, coagulopathies or infections. In this article, we review the main aspects of ALF, including the definition, diagnosis and complications. Also, we describe the standard-of-care strategies and recent advances in the treatment of ALF. Finally, we include our experience of care patients with ALF.
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Enfermedad Hepática Inducida por Sustancias y Drogas/terapia , Fallo Hepático Agudo/terapia , Acetaminofén/envenenamiento , Lesión Renal Aguda/etiología , Lesión Renal Aguda/terapia , Amanita , Analgésicos no Narcóticos/envenenamiento , Biopsia , Trastornos de la Coagulación Sanguínea/sangre , Trastornos de la Coagulación Sanguínea/etiología , Trastornos de la Coagulación Sanguínea/terapia , Edema Encefálico/prevención & control , Edema Encefálico/terapia , Circulación Extracorporea , Femenino , Hemorragia/etiología , Hemorragia/terapia , Hepatitis B/terapia , Hepatitis Autoinmune/terapia , Humanos , Hipertensión Intracraneal/etiología , Hipertensión Intracraneal/terapia , Hígado/patología , Fallo Hepático Agudo/complicaciones , Fallo Hepático Agudo/patología , Trasplante de Hígado , Intoxicación por Setas/terapia , Intercambio Plasmático , Embarazo , Complicaciones del Embarazo/terapia , Terapia de Reemplazo Renal , Respiración Artificial , Medición de Riesgo , Sepsis/etiología , Sepsis/terapia , Desintoxicación por Sorción , TromboelastografíaRESUMEN
OBJECTIVE: To examine the characteristics and outcomes of a multicenter patient cohort with indeterminate pediatric acute liver failure (IND-PALF) and with aplastic anemia with acute hepatitis treated with corticosteroids. STUDY DESIGN: Retrospective study of patients age 1-17 years with IND-PALF and aplastic anemia with acute hepatitis who presented between 2009 and 2018 to 1 of 4 institutions and were treated with corticosteroids for presumed immune dysregulation. RESULTS: Of 28 patients with IND-PALF (median of 4.0 years of age [range 1-16] and 71% male) 71% (n = 20) were treated with 0.5-4 mg/kg/day of intravenous methylprednisolone, and 8 patients received 10 mg/kg/day followed by a taper. By 21 days postcorticosteroid initiation, 14 patients (50%) underwent liver transplantation, 13 patients (46%) recovered with their native liver, and 1 patient (4%) died. Patients who recovered with their native liver received a median of 139 days (range 19-749) of corticosteroid therapy, with a median of 12 days (range 1-240) to international normalized ratio ≤1.2. Patients with aplastic anemia with acute hepatitis (n = 6; median of 9.5 years of age [range 1-12], 83% male), received 1-2 mg/kg/day of methylprednisolone for a median of 100 days (range 63-183), and all recovered with their native liver. One patient with IND-PALF and 2 patients with aplastic anemia with acute hepatitis developed a serious infection within 90 days postcorticosteroid initiation. CONCLUSIONS: Many patients with IND-PALF or aplastic anemia with acute hepatitis that were treated with corticosteroids improved, but survival with native liver may not be different from historical reports. A randomized controlled trial exploring the benefits and risks of steroid therapy is needed before it is adopted broadly.
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Anemia Aplásica/complicaciones , Glucocorticoides/uso terapéutico , Hepatitis/complicaciones , Fallo Hepático Agudo/complicaciones , Fallo Hepático Agudo/tratamiento farmacológico , Metilprednisolona/uso terapéutico , Enfermedad Aguda , Adolescente , Niño , Preescolar , Femenino , Humanos , Lactante , Masculino , Estudios Retrospectivos , Resultado del TratamientoRESUMEN
INTRODUCTION: Identification of predictive factors of mortality in a liver transplant (LT) program optimizes patient selection and allocation of organs. OBJECTIVE: To determine survival rates and predictive factors of mortality after LT in the National Liver Transplant Program of Uruguay. METHODS: A retrospective study was conducted analyzing data prospectively collected into a multidisciplinary database. All patients transplanted since the beginning of the program on July 2009 to April 2017 were included (n = 148). Twenty-nine factors were analyzed through the univariate Kaplan-Meier model. A Cox regression model was used in the multivariate analysis to identify the independent prognostic factors for survival. RESULTS: Overall survival was 92%, 87%, and 78% at discharge, 1 year, and 3 years, respectively. The Kaplan-Meier survival curves were significantly lower in: recipients aged >60 years, Model for End-Stage Liver Disease score >21, LT due to hepatocellular carcinoma (HCC) and acute liver failure (ALF), donors with comorbidities, intraoperative blood loss beyond the median (>2350 mL), red blood cell transfusion requirement beyond the median (>1254 mL), intraoperative complications, delay of extubation, invasive bacterial, and fungal infection after LT and stay in critical care unit >4 days. The Cox regression model (likelihood ratio test, P = 1.976 e-06) identified the following independent prognostic factors for survival: LT for HCC (hazard ratio [HR] 4.511; P = .001) and ALF (HR 6.346; P = .004), donors with comorbidities (HR 2.354; P = .041), intraoperative complications (HR 2.707; P = .027), and invasive fungal infections (HR 3.281; P = .025). CONCLUSION: The survival rates of LT patients as well as the mortality-associated factors are similar to those reported in the international literature.
Asunto(s)
Enfermedad Hepática en Estado Terminal/cirugía , Trasplante de Hígado/mortalidad , Adulto , Carcinoma Hepatocelular/complicaciones , Carcinoma Hepatocelular/cirugía , Enfermedad Hepática en Estado Terminal/etiología , Femenino , Humanos , Estimación de Kaplan-Meier , Fallo Hepático Agudo/complicaciones , Fallo Hepático Agudo/cirugía , Neoplasias Hepáticas/complicaciones , Neoplasias Hepáticas/cirugía , Trasplante de Hígado/efectos adversos , Masculino , Persona de Mediana Edad , Análisis Multivariante , Selección de Paciente , Modelos de Riesgos Proporcionales , Estudios Retrospectivos , Factores de Riesgo , Índice de Severidad de la Enfermedad , Tasa de Supervivencia , Uruguay/epidemiologíaRESUMEN
Hepatitis A virus (HAV) causes an acute infection and is usually asymptomatic in children. When clinical manifestations appear, these include choluria, jaundice, and abdominal pain. Although infrequent, extra-hepatic manifestations related to HAV have been described, affecting the heart, bone marrow, blood vessels, and other tissues.A 10-year-old boy from a rural area presented with a 15-day history of malaise, fever, and jaundice; laboratory examinations were compatible with HAV infection. The patient turned encephalopathic and was remitted to our center, where laboratory examinations showed a medullary aplasia and fulminant hepatitis requiring a liver transplant that was performed 72 hours after admission. At 24 hours post transplant, the patient developed a cardiomyopathy secondary to HAV, and intravenous immunoglobulin was administered. The patient is still alive and attending his medical check-ups.Although rare, extra-hepatic manifestations of HAV infection have been described in 14% of cases. The groups of patients affected are usually aged and present with high bilirubin levels. Acquired aplastic anemia and myocarditis caused by HAV are uncommon, and its pathophysiology has not yet been elucidated.HAV infection is usually asymptomatic in children, although extra-hepatic manifestations can appear requiring early detection and management.
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Anemia Aplásica/complicaciones , Cardiomiopatías/etiología , Hepatitis A/complicaciones , Inmunoglobulinas Intravenosas/uso terapéutico , Fallo Hepático Agudo/complicaciones , Cardiomiopatías/terapia , Niño , Hepatitis A/terapia , Humanos , Trasplante de Hígado , MasculinoRESUMEN
The consumption of botanicals for therapeutic purposes has increased significantly in recent years. Drug-induced liver disease (DILI) is a frequent cause of acute liver injury, around 50% in the United States, and about 1% is secondary to the use of phytotherapeuticals and herbal supplies. Ruellia bahiensis, a plant species of the Acanthaceae family, is a tropical plant distributed in Northeastern Brazil. In folk medicine in the state of Bahia, the species is known as "mãe-boa" and is commonly used. L.S.S, a 23-year old, female, patient was admitted at University Hospital of Bahia-Brazil with signs and symptoms of acute hepatitis. She had made daily use of an herbal supply popularly known as "mãe-boa" for at least two years prescribed by a physician. Diagnostic investigation was negative for viral and autoimmune hepatitis, leptospirosis, dengue, and CMV (cytomegalovirus). The patient had to undergo liver transplantation. Explant revealed massive hepatic necrosis. According to histological findings, and after exclusion of other etiologies, liver damage was assigned to herbal supply. The prolonged use of Ruellia bahiensis infusions may have caused the liver dysfunction.
Asunto(s)
Intoxicación por Plantas , Fallo Hepático Agudo/complicaciones , Trasplante de Hígado , Acanthaceae/clasificación , Medicamento Fitoterápico , Enfermedad Hepática Inducida por Sustancias y Drogas/clasificaciónRESUMEN
Intracranial hypertension and brain swelling are a major cause of morbidity and mortality of patients suffering from fulminant hepatic failure (FHF). The pathogenesis of these complications has been investigated in man, in experimental models and in isolated cell systems. Currently, the mechanism underlying cerebral edema and intracranial hypertension in the presence of FHF is multi-factorial in etiology and only partially understood. The aim of this paper is to review the pathophysiology of cerebral hemodynamic and metabolism changes in FHF in order to improve understanding of intracranial dynamics complication in FHF.
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Edema Encefálico/etiología , Circulación Cerebrovascular/fisiología , Hipertensión Intracraneal/etiología , Fallo Hepático Agudo/complicaciones , Edema Encefálico/fisiopatología , Encefalopatía Hepática/etiología , Encefalopatía Hepática/metabolismo , Encefalopatía Hepática/fisiopatología , Humanos , Hipertensión Intracraneal/fisiopatología , Fallo Hepático Agudo/metabolismo , Fallo Hepático Agudo/fisiopatologíaRESUMEN
ABSTRACT Intracranial hypertension and brain swelling are a major cause of morbidity and mortality of patients suffering from fulminant hepatic failure (FHF). The pathogenesis of these complications has been investigated in man, in experimental models and in isolated cell systems. Currently, the mechanism underlying cerebral edema and intracranial hypertension in the presence of FHF is multi-factorial in etiology and only partially understood. The aim of this paper is to review the pathophysiology of cerebral hemodynamic and metabolism changes in FHF in order to improve understanding of intracranial dynamics complication in FHF.
RESUMO O edema cerebral e a hipertensão intracraniana (HIC) são as principais causas de morbidade e mortalidade de pacientes com insuficiência hepática fulminante (IHF). A patogênese dessas complicações tem sido investigada no homem, em modelos experimentais e em sistemas celulares isolados. Atualmente, o mecanismo subjacente ao edema cerebral e HIC na presença de IHF é multifatorial em etiologia e pouco compreendido na literatura. O objetivo deste trabalho é revisar a fisiopatologia das alterações hemodinâmicas e metabólicas cerebrais na IHF, visando melhorar a compreensão da complicação da hemodinâmica encefálica na IHF.
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Humanos , Edema Encefálico/etiología , Circulación Cerebrovascular/fisiología , Fallo Hepático Agudo/complicaciones , Hipertensión Intracraneal/etiología , Edema Encefálico/fisiopatología , Encefalopatía Hepática/etiología , Encefalopatía Hepática/fisiopatología , Encefalopatía Hepática/metabolismo , Fallo Hepático Agudo/fisiopatología , Fallo Hepático Agudo/metabolismo , Hipertensión Intracraneal/fisiopatologíaRESUMEN
Introducción: la insuficiencia hepática fulminante (IHF) es un síndrome clínico poco frecuente, que se caracteriza por una disfunción hepática severa y repentina. La tioacetamida (TAA) es una hepatotoxina cuya administración puede inducir necrosis centrolobulillar en las células hepáticas y aumentar la formación de especies reactivas de oxígeno y la peroxidación lipídica en ratas. La glutamina es un precursor para la síntesis de glutatión. Objetivo: el objetivo del estudio es evaluar los efectos antioxidantes de la glutamina en un modelo de rata de IHF inducida por TAA. Métodos: ratas macho Wistar se dividieron en cuatro grupos de acuerdo con el tratamiento y el tiempo de evaluación: control, glutamina (25 mg/kg), tioacetamida (400 mg/kg) y tioacetamida más glutamina. Los animales se evaluaron después de 24, 36 y 48 horas. Se recogieron muestras de sangre para el análisis de los niveles de aspartato aminotransferasa (AST), alanina aminotransferasa (ALT), fosfatasa alcalina (AP), bilirrubina total (TB) y creatinina (CRE), y muestras de hígado para evaluar la peroxidación lipídica, las sustancias reactivas al ácido tiobarbitúrico (TBARS), la actividad de las enzimas antioxidantes superóxido dismutasa (SOD), glutatión peroxidasa (GPx), catalasa (CAT) y glutatión S-transferasa (GST). Además se midieron mediante inmunohistoquímica el factor nuclear kappa N (NF-κB), el fator de necrosis tumoral (TNF-α) y la óxido nítrico sintasa inducible (iNOS). Resultados: la TAA causó alteraciones en los parámetros bioquímicos e histológicos, y el aumento de los marcadores del proceso inflamatorio. Los niveles de TBARS y la actividad de SOD y GST fueron significativamente inferiores en los grupos de glutamina en comparación con TAA. La actividad de CAT se incrementó en los animales tratados con glutamina en comparación con la TAA. La actividad GPx también fue menor a las 36 y 48 h en los animales tratados com glutamina. El daño tisular y la expresión de NF-κB, TNF-α e iNOS fueron significativamente inferiores en los animales tratados con glutamina. Conclusión: la glutamina ha demostrado tener efectos protectores contra el daño hepático en un modelo de IHF inducida por TAA en la rata.
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Antioxidantes/farmacología , Glutamina/farmacología , Inflamación/tratamiento farmacológico , Fallo Hepático Agudo/tratamiento farmacológico , Estrés Oxidativo/efectos de los fármacos , Animales , Inflamación/etiología , Estimación de Kaplan-Meier , Peroxidación de Lípido/efectos de los fármacos , Hígado/metabolismo , Hígado/patología , Fallo Hepático Agudo/inducido químicamente , Fallo Hepático Agudo/complicaciones , Masculino , Ratas , Ratas Wistar , Especies Reactivas de Oxígeno/metabolismo , TioacetamidaRESUMEN
BACKGROUND: Pulmonary complications are common in acute liver failure (ALF). The role of the lungs in the uptake of harmful soluble endogenous macromolecules was evaluated in a porcine model of ALF induced by hepatic devascularization (n = 8) vs. controls (n = 8). In additional experiments, pulmonary uptake was investigated in healthy pigs. Fluorochrome-labeled modified albumin (MA) was applied to investigate the cellular uptake. RESULTS: As compared to controls, the ALF group displayed a 4-fold net increased lung uptake of hyaluronan, and 5-fold net increased uptake of both tissue plasminogen activator and lysosomal enzymes. Anatomical distribution experiments in healthy animals revealed that radiolabeled MA uptake (taken up by the same receptor as hyaluronan) was 53% by the liver, and 24% by the lungs. The lung uptake of LPS was 14% whereas 60% remained in the blood. Both fluorescence and electron microscopy revealed initial uptake of MA by pulmonary endothelial cells (PECs) with later translocation to pulmonary intravascular macrophages (PIMs). Moreover, the presence of PIMs was evident 10 min after injection. Systemic inflammatory markers such as leukopenia and increased serum TNF-α levels were evident after 20 min in the MA and LPS groups. CONCLUSION: Significant lung uptake of harmful soluble macromolecules compensated for the defect liver scavenger function in the ALF-group. Infusion of MA induced increased TNF-α serum levels and leukopenia, similar to the effect of the known inflammatory mediator LPS. These observations suggest a potential mechanism that may contribute to lung damage secondary to liver disease.
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Células Endoteliales/metabolismo , Fallo Hepático Agudo/metabolismo , Lesión Pulmonar/metabolismo , Pulmón/metabolismo , Animales , Transporte Biológico , Modelos Animales de Enfermedad , Fluoresceína-5-Isotiocianato/análogos & derivados , Fluoresceína-5-Isotiocianato/metabolismo , Ácido Hialurónico/metabolismo , Mediadores de Inflamación/sangre , Fallo Hepático Agudo/sangre , Fallo Hepático Agudo/complicaciones , Lesión Pulmonar/sangre , Lesión Pulmonar/etiología , Macrófagos Alveolares/metabolismo , Albúmina Sérica/metabolismo , Sus scrofa , Factores de TiempoRESUMEN
Acute liver failure is a critical medical condition defined as rapid development of hepatic dysfunction associated with encephalopathy. The prognosis in these patients is highly variable and depends on the etiology, interval between jaundice and encephalopathy, age, and the degree of coagulopathy. Determining the prognosis for this population is vital. Unfortunately, prognostic models with both high sensitivity and specificity for prediction of death have not been developed. Liver transplantation has dramatically improved survival in patients with acute liver failure. Still, 25% to 45% of patients will survive with medical treatment. The identification of patients who will eventually require liver transplantation should be carefully addressed through the combination of current prognostic models and continuous medical assessment. The concerns of inaccurate selection for transplantation are significant, exposing the recipient to a complex surgery and lifelong immunosuppression. In this challenging scenario, where organ shortage remains one of the main problems, alternatives to conventional orthotopic liver transplantation, such as living-donor liver transplantation, auxiliary liver transplant, and ABO-incompatible grafts, should be explored. Although overall outcomes after liver transplantation for acute liver failure are improving, they are not yet comparable to elective transplantation.
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Fallo Hepático Agudo/cirugía , Trasplante de Hígado/efectos adversos , Técnicas de Apoyo para la Decisión , Progresión de la Enfermedad , Humanos , Fallo Hepático Agudo/complicaciones , Fallo Hepático Agudo/diagnóstico , Fallo Hepático Agudo/mortalidad , Trasplante de Hígado/mortalidad , Selección de Paciente , Valor Predictivo de las Pruebas , Medición de Riesgo , Factores de Riesgo , Resultado del TratamientoRESUMEN
The most important topics in fulminant hepatic failure are cerebral edema and intracranial hypertension. Among all therapeutic options, systemic induced hypothermia to 33 - 34ºC has been reported to reduce the high pressure and increase the time during which patients can tolerate a graft. This review discusses the indications and adverse effects of hypothermia.
Asunto(s)
Hipotermia Inducida/métodos , Fallo Hepático Agudo/terapia , Trasplante de Hígado/métodos , Edema Encefálico/etiología , Edema Encefálico/prevención & control , Humanos , Hipertensión Intracraneal/etiología , Hipertensión Intracraneal/prevención & control , Fallo Hepático Agudo/complicacionesRESUMEN
Os tópicos mais importantes na falência hepática fulminante são o edema cerebral e a hipertensão intracraniana. Dentre todas as opções terapêuticas, tem sido relatado que a hipotermia sistêmica induzida em níveis entre 33 - 34ºC reduz a elevação da pressão e aumenta o tempo durante o qual os pacientes podem tolerar um enxerto. Esta revisão discutiu as indicações e os efeitos adversos da hipotermia.
The most important topics in fulminant hepatic failure are cerebral edema and intracranial hypertension. Among all therapeutic options, systemic induced hypothermia to 33 - 34ºC has been reported to reduce the high pressure and increase the time during which patients can tolerate a graft. This review discusses the indications and adverse effects of hypothermia.
Asunto(s)
Humanos , Trasplante de Hígado/métodos , Fallo Hepático Agudo/terapia , Hipotermia Inducida/métodos , Edema Encefálico/etiología , Edema Encefálico/prevención & control , Fallo Hepático Agudo/complicaciones , Hipertensión Intracraneal/etiología , Hipertensión Intracraneal/prevención & controlAsunto(s)
Acetilcisteína/uso terapéutico , Glucocorticoides/uso terapéutico , Fallo Hepático Agudo/tratamiento farmacológico , Prednisona/uso terapéutico , Síndrome de Hipersensibilidad a Medicamentos/complicaciones , Femenino , Humanos , Fallo Hepático Agudo/complicaciones , Persona de Mediana Edad , Inducción de RemisiónAsunto(s)
Fallo Hepático Agudo/complicaciones , Fallo Hepático Agudo/diagnóstico , Fallo Hepático Agudo/terapia , Vena Porta/anomalías , Malformaciones Vasculares/complicaciones , Malformaciones Vasculares/diagnóstico , Malformaciones Vasculares/terapia , Embolización Terapéutica/métodos , Infecciones por Enterovirus/diagnóstico , Humanos , Hiperamonemia/diagnóstico , Hiperbilirrubinemia/diagnóstico , Recién Nacido , Hígado/diagnóstico por imagen , Hígado/patología , Masculino , Tomografía Computarizada por Rayos X , Resultado del Tratamiento , UltrasonografíaRESUMEN
BACKGROUND AND AIMS. Acute-on-chronic liver failure has been recognized as a sudden deterioration of cirrhosis, with a high short-term mortality. Prognostic scores are used to assess liver dysfunction. However, there is not enough information on a score to predict short term mortality in those patients. We aimed to investigate the prognostic value of bilirubin concentration in predicting the 1-week outcome of patients with acute-on-chronic liver failure. MATERIAL AND METHODS. We performed a retrospective analysis with a cohort of 65 patients (33 women/32 men), age average of 64 years, diagnosed with acute-on-chronic liver failure with at least 1 week follow-up. Demographics, clinical and biochemical variables were analyzed. Most patients died (59 %) within 1 week of follow-up. RESULTS. In univariate logistic regression analysis, admission to the intensive care unit, use of vasoactive drugs, need for parenteral nutrition, and levels of conjugated, unconjugated, and total bilirubin at the time of hospital admission were significantly associated with 1-week mortality; in a multivariate logistic regression, conjugated (p = 0.01), unconjugated (p =0.01), and total bilirubin (p = 0.009) were independently associated with 1-week mortality. In ROC curve analysis, conjugated (0.751, p < 0.05) and total bilirubin (0.746, p < 0.05) levels were significantly the best short-term mortality predictors. CONCLUSIONS. High levels of bilirubin are able to predict short-term mortality in these patients. Also, we suggest that bilirubin can be used as a biochemical marker to improve triage of patients with acute-on-chronic liver failure especially with emerging interventions such as extracorporeal liver assist devices and possibly improved early phase pharmacological therapies.
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Bilirrubina/sangre , Enfermedad Hepática en Estado Terminal/sangre , Cirrosis Hepática/sangre , Fallo Hepático Agudo/sangre , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Biomarcadores/sangre , Estudios de Cohortes , Enfermedad Hepática en Estado Terminal/complicaciones , Enfermedad Hepática en Estado Terminal/mortalidad , Femenino , Humanos , Unidades de Cuidados Intensivos/estadística & datos numéricos , Cirrosis Hepática/complicaciones , Cirrosis Hepática/mortalidad , Fallo Hepático Agudo/complicaciones , Fallo Hepático Agudo/mortalidad , Modelos Logísticos , Masculino , Persona de Mediana Edad , Análisis Multivariante , Nutrición Parenteral/estadística & datos numéricos , Pronóstico , Estudios Retrospectivos , Adulto JovenRESUMEN
Although the etiologies of pediatric acute liver failure (ALF) are diverse, ultimate pathophysiologic pathways and management challenges for these disorders, usually lethal in the pre-transplant era, are similar. This review considers particularly the mechanisms of, and monitoring for, intracranial hypertension and coagulopathy; summarizes detailed advice for management of the ALF-associated failures of multiple body systems; and reviews the variety of prognostic scores available to guide management and assist in choosing the patients most apt to benefit from liver transplantation and the optimal timing for such transplantation.
Asunto(s)
Fallo Hepático Agudo/terapia , Trastornos de la Coagulación Sanguínea/etiología , Niño , Encefalopatía Hepática/diagnóstico , Encefalopatía Hepática/terapia , Humanos , Presión Intracraneal/fisiología , Fallo Hepático Agudo/complicaciones , Fallo Hepático Agudo/diagnóstico , Trasplante de Hígado , Monitoreo Fisiológico/métodos , Selección de Paciente , PronósticoRESUMEN
This is the first report presenting a human immunodeficiency virus (HIV)-positive patient with fulminant hepatic failure receiving a liver graft from a Chagas disease-seropositive deceased donor. We describe the history of a 38-year-old HIV-positive female patient who developed fulminant hepatic failure of an autoimmune etiology with rapid deterioration of her clinical status and secondary multiorgan failure and, therefore, needed emergency liver transplantation (LT) as a lifesaving procedure. Because of the scarcity of organs and the high mortality rate for emergency status patients on the LT waiting list, we decided to accept a Chagas disease-seropositive deceased donor liver graft for this immunocompromised Chagas disease-seronegative patient. The recipient had a rapid postoperative recovery and was discharged on postoperative day 9 without prophylactic treatment for Chagas disease. Fifteen months after LT, she was still alive and had never experienced seroconversion on periodic screening tests for Chagas detection. Although there is an inherent risk of acute Chagas disease developing in seronegative recipients, our report suggests that these infected organs can be safely used as a lifesaving strategy for HIV patients with a high need for LT.