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 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

OBJECTIVES: To determine risk factors of mortality in the preoperative, perioperative, and immediate postoperative period of a pediatric population that has undergone orthotopic liver transplantation for fulminant hepatic failure in a pediatric intensive care unit. DESIGN: Retrospective review of medical records. SETTING: A pediatric intensive care unit in a children's hospital. PATIENTS: Sixty patients with fulminant hepatic failure who fulfilled King's College criteria for liver transplantation. INTERVENTION: Orthotopic liver transplantation was performed according to standard techniques. Before transplantation, patients were admitted to a pediatric intensive care unit when intensive care was required, and patients were always admitted to a pediatric intensive care unit after the operation. Measurements: A total of 20 variables were studied via univariate and multivariate analysis; statistical significance was accepted when p </=.05. MAIN RESULTS: A total of 70 orthotopic liver transplantations were performed in 60 children (mean age, 64.11 +/- 40.97 months; range, 11 months to 14 yrs) for fulminant hepatic failure. Fulminant hepatic failure was caused by hepatitis A virus in 60% of cases, and non-A non-B non-C hepatitis was responsible in 40% of cases. Univariate analysis showed that the complications of infectious, hemodynamic, renal, and gastrointestinal bleeding are significant variables. Posttransplant respiratory support was also a significant variable. When the same variables were calculated with a multivariate analysis, no significant results were obtained. Multivariate analysis showed that mortality risk factors in this population were: etiology of liver failure (p <.002), liver size (p <.014), ischemia time (p <.041), ventilatory support before transplantation (p <.048), neurologic complications after orthotopic liver transplantation (p <.003), and acute rejection (p <.021). CONCLUSIONS: Hepatitis A virus is the major cause of fulminant liver failure in Argentina, but non-A non-B non-C hepatitis is an independent risk factor of mortality. Reduced-size graft, longer ischemia time, ventilatory support before orthotopic liver transplantation, neurologic complications, and acute rejection after transplantation are independent predictive factors of mortality. Better sanitary conditions and universal immunization for hepatitis A virus should reduce hepatitis A virus and hepatitis A virus-induced fulminant hepatic failure.
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PMID:Mortality risk factors of a pediatric population with fulminant hepatic failure undergoing orthotopic liver transplantation in a pediatric intensive care unit. 1278 Sep 61

Acute liver failure (ALF) is a rare but challenging clinical syndrome with multiple causes; a specific etiology cannot be identified in 15% of adult and 50% of pediatric cases. The course of ALF is variable and the mortality rate is high. Liver transplantation is the only therapy of proven benefit, but the rapidity of progression and the variable course of ALF limit its use. Currently in the United States, spontaneous survival occurs in approximately 45%, liver transplantation in 25%, and death without transplantation in 30% of adults with ALF. Higher rates of spontaneous recovery (56%) and transplantation (31%) with lower rates of death (13%) occur in children. The outcome of ALF varies by etiology, favorable prognoses being found with acetaminophen overdose, hepatitis A, and ischemia (approximately 60% spontaneous survival), and poor prognoses with drug-induced ALF, hepatitis B, and indeterminate cases (approximately 25% spontaneous survival). Excellent intensive care is critical in management of patients with ALF. Nonspecific therapies are of unproven benefit. Future possible therapeutic approaches include N-acetylcysteine, hypothermia, liver assist devices, and hepatocyte transplantation. Advances in stem cell research may allow provision of cells for bioartificial liver support. ALF presents many challenging opportunities in both clinical and basic research.
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PMID:Acute liver failure: Summary of a workshop. 1831 40

Chest pain requires a detailed differential diagnosis with good history-taking skills to differentiate between cardiogenic and noncardiogenic causes. Moreover, when other symptoms such as fever and elevated white blood cell count are involved, it may be necessary to consider causes that include infectious sources. A 53-year-old female with no significant past medical history returned to the hospital with recurrent complaints of chest pain that was constant, substernal, reproducible, and exacerbated with inspiration and expiration. The chest pain was thought to be noncardiogenic, as electrocardiography did not demonstrate changes, and cardiac enzymes were found to be negative for signs of ischemia. The patient's blood cultures were analyzed from a previous admission and were shown to be positive for Staphylococcus aureus. The patient was started empirically on vancomycin, which was later switched to ceftriaxone as the bacteria were more sensitive to this antibiotic. A transthoracic echocardiogram did not demonstrate any vegetation or signs of endocarditis. There was a small right pleural effusion discovered on X-ray. Therefore, computed tomography as well as magnetic resonance imaging of the chest were performed, and showed osteomyelitis of the chest. The patient was continued on intravenous ceftriaxone for a total of 6 weeks. Tests for HIV, hepatitis A, B, and C were all found to be negative. The patient had no history of childhood illness, recurrent infections, or previous trauma to the chest, and had had no recent respiratory infections, pneumonia, or any underlying lung condition. Hence, her condition was thought to be a case of primary sternal osteomyelitis without known cause.
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PMID:Another cause of chest pain: Staphylococcus aureus sternal osteomyelitis in an otherwise healthy adult. 2524 11

Acute kidney injury (AKI) currently is diagnosed by a temporal trend of a single blood analyte: serum creatinine. This measurement is neither sensitive nor specific to kidney injury or its protean forms. Newer biomarkers, neutrophil gelatinase-associated lipocalin (NGAL, Lipocalin 2, Siderocalin), or kidney injury molecule-1 (KIM-1, Hepatitis A Virus Cellular Receptor 1), accelerate the diagnosis of AKI as well as prospectively distinguish rapidly reversible from prolonged causes of serum creatinine increase. Nonetheless, these biomarkers lack the capacity to subfractionate AKI further (eg, sepsis versus ischemia versus nephrotoxicity from medications, enzymes, or metals) or inform us about the primary and secondary sites of injury. It also is unknown whether all nephrons are injured in AKI, whether all cells in a nephron are affected, and whether injury responses can be stimulus-specific or cell type-specific or both. In this review, we summarize fully agnostic tissue interrogation approaches that may help to redefine AKI in cellular and molecular terms, including single-cell and single-nuclei RNA sequencing technology. These approaches will empower a shift in the current paradigm of AKI diagnosis, classification, and staging, and provide the renal community with a significant advance toward precision medicine in the analysis AKI.
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PMID:Precision Medicine for Acute Kidney Injury (AKI): Redefining AKI by Agnostic Kidney Tissue Interrogation and Genetics. 2929 61

Acute liver failure (ALF) can be due to numerous causes and result in fatality or necessitate liver transplantation if left untreated. Possible etiologies of ALF include ischemia, venous obstruction, medications, toxins, autoimmune hepatitis, metabolic and infectious causes including hepatitis A-E, varicella-zoster virus (VZV), cytomegalovirus (CMV), herpes simplex virus (HSV), Epstein-Barr virus (EBV), and adenovirus with VZV being the most rarely reported. Pathognomonic skin lesions facilitate diagnosis of VZV hepatitis, but definitive diagnosis is secured with liver biopsy, tissue histopathology, culture, and specific VZV polymerase chain reaction (PCR). Antiviral treatment with intravenous acyclovir can be effective if initiated in a timely manner; however, comorbidities and complications frequently result in high mortality, especially in immunocompromised hosts as exemplified in this case presentation.
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PMID:Acute Liver Failure due to Disseminated Varicella Zoster Infection. 3036 7