ABSTRACT
BACKGROUND: Postoperative severe cardiopulmonary failure carries a high rate of mortality. Extracorporeal membrane oxygenation (ECMO) can be used as a salvage therapy when conventional therapies fail. METHODS: We retrospectively reviewed our experience with ECMO support in the early postoperative period after liver transplant between September 2011 and May 2016. RESULTS: Out of 537 liver transplants performed at our institution, seven patients required ECMO support with a median age of 52 and a median MELD score of 28. Veno-venous ECMO was used in four patients with severe respiratory failure while the rest required veno-arterial ECMO for circulatory failure. The median time from transplant to cannulation was 3 days with a median duration of ECMO support of 7 days. All patients except one were successfully decannulated. The median hospital length of stay was 58 days with an in-hospital mortality of 28.6%. CONCLUSION: Extracorporeal membrane oxygenation can be considered a viable rescue therapy in the setting of severe postoperative cardiopulmonary failure. Extracorporeal membrane oxygenation therapy was successful in saving patients who were otherwise unsalvageable.
Subject(s)
Extracorporeal Membrane Oxygenation/methods , Graft Rejection/therapy , Heart Arrest/therapy , Hospital Mortality/trends , Liver Transplantation/adverse effects , Postoperative Complications/therapy , Respiratory Insufficiency/therapy , Adult , Female , Follow-Up Studies , Graft Rejection/etiology , Graft Rejection/mortality , Graft Survival , Heart Arrest/etiology , Heart Arrest/mortality , Humans , Male , Middle Aged , Postoperative Complications/etiology , Postoperative Complications/mortality , Respiratory Insufficiency/etiology , Respiratory Insufficiency/mortality , Retrospective Studies , Survival Rate , Treatment OutcomeABSTRACT
The drivers and the specification of CD4+ T cell differentiation in the tumor microenvironment and their contributions to tumor immunity or tolerance are incompletely understood. Using models of pancreatic ductal adenocarcinoma (PDA), we show that a distinct subset of tumor-infiltrating dendritic cells (DC) promotes PDA growth by directing a unique TH-program. Specifically, CD11b+CD103- DC predominate in PDA, express high IL-23 and TGF-ß, and induce FoxP3neg tumor-promoting IL-10+IL-17+IFNγ+ regulatory CD4+ T cells. The balance between this distinctive TH program and canonical FoxP3+ TREGS is unaffected by pattern recognition receptor ligation and is modulated by DC expression of retinoic acid. This TH-signature is mimicked in human PDA where it is associated with immune-tolerance and diminished patient survival. Our data suggest that CD11b+CD103- DC promote CD4+ T cell tolerance in PDA which may underscore its resistance to immunotherapy.
Subject(s)
Dendritic Cells/immunology , Interleukin-10/metabolism , Interleukin-17/metabolism , Pancreatic Neoplasms/immunology , T-Lymphocytes, Regulatory/immunology , Adenocarcinoma/genetics , Adenocarcinoma/immunology , Adenocarcinoma/pathology , Animals , Carcinoma, Pancreatic Ductal/genetics , Carcinoma, Pancreatic Ductal/immunology , Carcinoma, Pancreatic Ductal/pathology , Cell Differentiation , Disease Progression , Forkhead Transcription Factors , Gene Expression Regulation, Neoplastic , Humans , Lectins, C-Type/metabolism , Mice, Inbred C57BL , Pancreatic Neoplasms/genetics , Pancreatic Neoplasms/pathology , Phenotype , Signal Transduction , Th17 Cells/immunology , Toll-Like Receptor 2/metabolism , Tretinoin/metabolism , Pancreatic NeoplasmsABSTRACT
N-Acetylcysteine (NAC) is reported to have multiple clinical applications in addition to being the specific antidote for acetaminophen toxicity. NAC stimulates glutathione biosynthesis, promotes detoxification, and acts directly as a scavenger of free radicals. It is a powerful antioxidant and a potential treatment option for diseases characterized by the generation of free oxygen radicals. We present a case of postoperative hepatic dysfunction of multifactorial etiology in a patient with therapeutic acetaminophen levels, where hepatic function improved considerably following administration of intravenous NAC. This case suggests that NAC should be considered for treatment of acute liver dysfunction in the postoperative setting, even in the absence of elevated acetaminophen levels.
