Multiple Organ Failure

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Joseph A Carcillo - One of the best experts on this subject based on the ideXlab platform.

  • a multicenter network assessment of three inflammation phenotypes in pediatric sepsis induced Multiple Organ Failure
    Pediatric Critical Care Medicine, 2019
    Co-Authors: Joseph A Carcillo, Mark W Hall, Robert A Berg, David L Wessel, Murray M Pollack, Kathleen L Meert, Christopher J L Newth, John C Lin, Allan Doctor, Tom Shanley
    Abstract:

    OBJECTIVES Ongoing adult sepsis clinical trials are assessing therapies that target three inflammation phenotypes including 1) immunoparalysis associated, 2) thrombotic microangiopathy driven thrombocytopenia associated, and 3) sequential liver Failure associated Multiple Organ Failure. These three phenotypes have not been assessed in the pediatric multicenter setting. We tested the hypothesis that these phenotypes are associated with increased macrophage activation syndrome and mortality in pediatric sepsis. DESIGN Prospective severe sepsis cohort study comparing children with Multiple Organ Failure and any of these phenotypes to children with Multiple Organ Failure without these phenotypes and children with single Organ Failure. SETTING Nine PICUs in the Eunice Kennedy Shriver National Institutes of Child Health and Human Development Collaborative Pediatric Critical Care Research Network. PATIENTS Children with severe sepsis and indwelling arterial or central venous catheters. INTERVENTIONS Clinical data collection and twice weekly blood sampling until PICU day 28 or discharge. MEASUREMENTS AND MAIN RESULTS Of 401 severe sepsis cases enrolled, 112 (28%) developed single Organ Failure (0% macrophage activation syndrome 0/112; < 1% mortality 1/112), whereas 289 (72%) developed Multiple Organ Failure (9% macrophage activation syndrome 24/289; 15% mortality 43/289). Overall mortality was higher in children with Multiple Organ and the phenotypes (24/101 vs 20/300; relative risk, 3.56; 95% CI, 2.06-6.17). Compared to the 188 Multiple Organ Failure patients without these inflammation phenotypes, the 101 Multiple Organ Failure patients with these phenotypes had both increased macrophage activation syndrome (19% vs 3%; relative risk, 7.07; 95% CI, 2.72-18.38) and mortality (24% vs 10%; relative risk, 2.35; 95% CI, 1.35-4.08). CONCLUSIONS These three inflammation phenotypes were associated with increased macrophage activation syndrome and mortality in pediatric sepsis-induced Multiple Organ Failure. This study provides an impetus and essential baseline data for planning multicenter clinical trials targeting these inflammation phenotypes in children.

  • three hypothetical inflammation pathobiology phenotypes and pediatric sepsis induced Multiple Organ Failure outcome
    Pediatric Critical Care Medicine, 2017
    Co-Authors: Joseph A Carcillo, Trung C. Nguyen, Mark W Hall, Scott E Halstead, Ron W Reeder, Rajesh Aneja, Bita Shakoory, Dennis W Simon
    Abstract:

    Objectives:We hypothesize that three inflammation pathobiology phenotypes are associated with increased inflammation, proclivity to develop features of macrophage activation syndrome, and Multiple Organ Failure-related death in pediatric severe sepsis.Design:Prospective cohort study comparing childr

  • use of therapeutic plasma exchange in children with thrombocytopenia associated Multiple Organ Failure in the turkish thrombocytopenia associated Multiple Organ Failure network
    Pediatric Critical Care Medicine, 2014
    Co-Authors: Esra Sevketoglu, Dincer Yildizdas, Ozden Ozgur Horoz, Hasan Serdar Kihtir, Tanil Kendirli, Suleyman Bayraktar, Joseph A Carcillo
    Abstract:

    OBJECTIVE Thrombocytopenia-associated Multiple Organ Failure can lead to high mortality in critically ill children, possibly related to consequences of thrombotic microangiopathy. Plasma exchange therapy may improve thrombotic microangiopathy. The purpose of this observational cohort study is to describe whether there is an association between use of plasma exchange therapy and outcome in the Turkish thrombocytopenia-associated Multiple Organ Failure network. SETTING-INTERVENTIONS We performed a retrospective cohort analysis in patients with thrombocytopenia-associated Multiple Organ Failure at three different PICUs comparing those who received plasma exchange (+) plus standard therapies with those who did not receive plasma exchange (-) and only received standard therapies. RESULTS Among 42 of the enrolled patients with thrombocytopenia-associated Multiple Organ Failure, all had a primary or secondary sepsis diagnosis. Fifteen received plasma exchange therapy (PE [+] group) and 27 received standard medical treatment without plasma exchange (PE [-] group). The mean age was 17.69 months (8.24-54.22) in the PE (+) group and 13.46 months (6.47-20.55) in the PE (-) group. Age (p = 0.232), gender (p = 0.206), thrombocyte count (p = 0.09), Organ Failure Index score (p = 0.111), and pediatric logistic Organ dysfunction score (p = 0.177) at admission were not statistically different between groups. The overall 28-day mortality was higher in the PE (-) group (70.37%) compared with the PE (+) group (26.67%) (univariate p = 0.006; multivariate controlling for pediatric logistic Organ dysfunction, Organ Failure Index, Pediatric Risk of Mortality scores, and neurological Failure p = 0.048). Length of stay was increased in the PE (+) group (p = 0.004). CONCLUSIONS The positive association found between use of plasma exchange therapy and improved survival supports the potential of this therapy in Turkish children with thrombocytopenia-associated Multiple Organ Failure. The positive, although less so, associated treatment effect observed after controlling for illness severity provides further rationale for performing a randomized controlled trial in the pediatric Turkish thrombocytopenia-associated Multiple Organ Failure network. Sample size calculations call for a 100-patient trial with a pre hoc interim analysis after enrollment of 50 patients with thrombocytopenia-associated Multiple Organ Failure.

  • Thrombocytopenia-Associated Multiple Organ Failure Syndrome
    Pediatric Critical Care Medicine, 2014
    Co-Authors: Trung C. Nguyen, Yong Y. Han, James D. Fortenberry, Zhou Zhou, Miguel A. Cruz, Joseph A Carcillo
    Abstract:

    Thrombocytopenia-associated Multiple Organ Failure (TAMOF) is a clinical syndrome often managed by critical care physicians. It is characterized by new onset thrombocytopenia in the setting of evolving Multiple Organ Failure. TAMOF is an entity within the family of thrombotic microangiopathies, a spectrum of mixed coagulopathies and thrombotic disorders that include thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS) on one end of the spectrum and disseminated intravascular coagulation (DIC) on the other. Autopsies performed in patients who have succumbed to DIC, TTP and HUS reveal disseminated microvascular thromboses with distinct findings that help to differentiate these three entities. Furthermore, our biologic and molecular understanding of the pathophysiologic processes governing DIC, TTP and HUS have significantly expanded and allow better laboratory delineation among these three entities. Tissue factor plays a pivotal role in the initiation and propagation of DIC. Von Willebrand factors and deficient ADAMTS-13 (a.k.a von Willebrand factor-cleaving proteinase) drive the pathology in TTP. Shiga toxins and the complement pathway drive the pathology in HUS. With better understanding of the biology of TAMOF syndrome, innovative therapies are currently being evaluated with the hope of reversing this destructive pathology.

  • pediatric septic shock and Multiple Organ Failure
    Critical Care Clinics, 2003
    Co-Authors: Joseph A Carcillo
    Abstract:

    In the last 5 years, the understanding of the epidemiology and pathogenesis of pediatric sepsis, septic shock, and Multiple Organ Failure has expanded greatly. There has also been a substantial increase in the number of successful randomized trials in which success has been measured as reduction in mortality in adults, children, and newborns. This article discusses these advances, updating the 1997 article on septic shock written by the author and by Dr. Robert E. Cunnion and following the format of the 1997 article.

Mark W Hall - One of the best experts on this subject based on the ideXlab platform.

  • a multicenter network assessment of three inflammation phenotypes in pediatric sepsis induced Multiple Organ Failure
    Pediatric Critical Care Medicine, 2019
    Co-Authors: Joseph A Carcillo, Mark W Hall, Robert A Berg, David L Wessel, Murray M Pollack, Kathleen L Meert, Christopher J L Newth, John C Lin, Allan Doctor, Tom Shanley
    Abstract:

    OBJECTIVES Ongoing adult sepsis clinical trials are assessing therapies that target three inflammation phenotypes including 1) immunoparalysis associated, 2) thrombotic microangiopathy driven thrombocytopenia associated, and 3) sequential liver Failure associated Multiple Organ Failure. These three phenotypes have not been assessed in the pediatric multicenter setting. We tested the hypothesis that these phenotypes are associated with increased macrophage activation syndrome and mortality in pediatric sepsis. DESIGN Prospective severe sepsis cohort study comparing children with Multiple Organ Failure and any of these phenotypes to children with Multiple Organ Failure without these phenotypes and children with single Organ Failure. SETTING Nine PICUs in the Eunice Kennedy Shriver National Institutes of Child Health and Human Development Collaborative Pediatric Critical Care Research Network. PATIENTS Children with severe sepsis and indwelling arterial or central venous catheters. INTERVENTIONS Clinical data collection and twice weekly blood sampling until PICU day 28 or discharge. MEASUREMENTS AND MAIN RESULTS Of 401 severe sepsis cases enrolled, 112 (28%) developed single Organ Failure (0% macrophage activation syndrome 0/112; < 1% mortality 1/112), whereas 289 (72%) developed Multiple Organ Failure (9% macrophage activation syndrome 24/289; 15% mortality 43/289). Overall mortality was higher in children with Multiple Organ and the phenotypes (24/101 vs 20/300; relative risk, 3.56; 95% CI, 2.06-6.17). Compared to the 188 Multiple Organ Failure patients without these inflammation phenotypes, the 101 Multiple Organ Failure patients with these phenotypes had both increased macrophage activation syndrome (19% vs 3%; relative risk, 7.07; 95% CI, 2.72-18.38) and mortality (24% vs 10%; relative risk, 2.35; 95% CI, 1.35-4.08). CONCLUSIONS These three inflammation phenotypes were associated with increased macrophage activation syndrome and mortality in pediatric sepsis-induced Multiple Organ Failure. This study provides an impetus and essential baseline data for planning multicenter clinical trials targeting these inflammation phenotypes in children.

  • therapeutic plasma exchange in children with thrombocytopenia associated Multiple Organ Failure the thrombocytopenia associated Multiple Organ Failure network prospective experience
    Critical Care Medicine, 2019
    Co-Authors: James D. Fortenberry, Trung Nguyen, Jocelyn R Grunwell, Rajesh K Aneja, Derek S Wheeler, Mark W Hall, Geoffrey M Fleming, Rod Tarrago, Sandra D W Buttram
    Abstract:

    Objective:The objective was to compare the resolution of Organ dysfunction, 28-day mortality, and biochemical markers in children with thrombocytopenia-associated Multiple Organ Failure who received therapeutic plasma exchange versus no therapeutic plasma exchange.Design:Observational longitudinal c

  • three hypothetical inflammation pathobiology phenotypes and pediatric sepsis induced Multiple Organ Failure outcome
    Pediatric Critical Care Medicine, 2017
    Co-Authors: Joseph A Carcillo, Trung C. Nguyen, Mark W Hall, Scott E Halstead, Ron W Reeder, Rajesh Aneja, Bita Shakoory, Dennis W Simon
    Abstract:

    Objectives:We hypothesize that three inflammation pathobiology phenotypes are associated with increased inflammation, proclivity to develop features of macrophage activation syndrome, and Multiple Organ Failure-related death in pediatric severe sepsis.Design:Prospective cohort study comparing childr

  • Microvascular thrombosis in pediatric Multiple Organ Failure: Is it a therapeutic target?
    Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Car, 2001
    Co-Authors: Trung Nguyen, Mark W Hall, Yong Han, Melinda Fiedor, Andrea Hasset, Ileana Lopez-plaza, Scott Watson, Lucy Chai See Lum, Joseph A Carcillo
    Abstract:

    PURPOSE: To discuss the current rationale for the use of specific and nonspecific therapies for thrombotic microangiopathy in thrombocytopenia-associated pediatric Multiple Organ Failure syndromes. Methods: Pertinent PubMed and MEDLINE citations and proceedings of recent critical care meeting presentations were reviewed. RESULTS: Critical care clinicians have reported using antithrombin III concentrate, protein C concentrate, activated protein C, prostacyclin and its analogues, heparin, tissue factor pathway inhibitor concentrate, plasma infusion, plasma exchange, whole blood exchange, pentoxifylline, tissue plasminogen activator, urokinase, and streptokinase with perceived therapeutic benefits in patients with thrombocytopenia-associated Multiple Organ Failure, including those with thrombotic thrombocytopenic purpura/hemolytic uremic syndrome, disseminated intravascular coagulation syndrome, and secondary thrombotic microangiopathy syndrome without prolonged prothrombin time/activated partial thromboplastin time. CONCLUSION: Assuming that underlying disease is remediable, a consensus has developed that thrombotic microangiopathy is a therapeutic target in children with thrombocytopenia-associated Multiple Organ Failure syndromes. Studies are warranted to delineate efficacious use of specific and nonspecific therapies to prevent and reverse thrombotic microangiopathy in these patients.

Tom Shanley - One of the best experts on this subject based on the ideXlab platform.

  • a multicenter network assessment of three inflammation phenotypes in pediatric sepsis induced Multiple Organ Failure
    Pediatric Critical Care Medicine, 2019
    Co-Authors: Joseph A Carcillo, Mark W Hall, Robert A Berg, David L Wessel, Murray M Pollack, Kathleen L Meert, Christopher J L Newth, John C Lin, Allan Doctor, Tom Shanley
    Abstract:

    OBJECTIVES Ongoing adult sepsis clinical trials are assessing therapies that target three inflammation phenotypes including 1) immunoparalysis associated, 2) thrombotic microangiopathy driven thrombocytopenia associated, and 3) sequential liver Failure associated Multiple Organ Failure. These three phenotypes have not been assessed in the pediatric multicenter setting. We tested the hypothesis that these phenotypes are associated with increased macrophage activation syndrome and mortality in pediatric sepsis. DESIGN Prospective severe sepsis cohort study comparing children with Multiple Organ Failure and any of these phenotypes to children with Multiple Organ Failure without these phenotypes and children with single Organ Failure. SETTING Nine PICUs in the Eunice Kennedy Shriver National Institutes of Child Health and Human Development Collaborative Pediatric Critical Care Research Network. PATIENTS Children with severe sepsis and indwelling arterial or central venous catheters. INTERVENTIONS Clinical data collection and twice weekly blood sampling until PICU day 28 or discharge. MEASUREMENTS AND MAIN RESULTS Of 401 severe sepsis cases enrolled, 112 (28%) developed single Organ Failure (0% macrophage activation syndrome 0/112; < 1% mortality 1/112), whereas 289 (72%) developed Multiple Organ Failure (9% macrophage activation syndrome 24/289; 15% mortality 43/289). Overall mortality was higher in children with Multiple Organ and the phenotypes (24/101 vs 20/300; relative risk, 3.56; 95% CI, 2.06-6.17). Compared to the 188 Multiple Organ Failure patients without these inflammation phenotypes, the 101 Multiple Organ Failure patients with these phenotypes had both increased macrophage activation syndrome (19% vs 3%; relative risk, 7.07; 95% CI, 2.72-18.38) and mortality (24% vs 10%; relative risk, 2.35; 95% CI, 1.35-4.08). CONCLUSIONS These three inflammation phenotypes were associated with increased macrophage activation syndrome and mortality in pediatric sepsis-induced Multiple Organ Failure. This study provides an impetus and essential baseline data for planning multicenter clinical trials targeting these inflammation phenotypes in children.

Robert H. Bartlett - One of the best experts on this subject based on the ideXlab platform.

  • Continuous renal replacement therapy in Multiple Organ Failure
    American Journal of Kidney Diseases, 1996
    Co-Authors: Robert H. Bartlett
    Abstract:

    Abstract Intermittent hemodialysis is excellent renal replacement therapy for isolated acute renal Failure. Continuous hemodiafiltration is preferred in Multiple Organ Failure because of stable hemodynamics, full feeding and fluid infusion, and ease of use in the septic or hypotensive patient. Recovery from Multiple Organ Failure is improving in the University of Michigan Surgical Intensive Care Unit (SICU) over the last 10 years. One factor is the use of continuous renal replacement therapy facilitating full nutrition.

Sandra D W Buttram - One of the best experts on this subject based on the ideXlab platform.