677: FATAL MULTIORGAN FAILURE AND SEPTIC SHOCK DUE TO DISSEMINATED COCCIDIOIDOMYCOSIS

2018 ◽  
Vol 46 (1) ◽  
pp. 325-325
Author(s):  
Isaac McCool ◽  
John Walsh ◽  
Alexandra Perry ◽  
Ryan Maves
2018 ◽  
Vol 46 (1) ◽  
pp. 695-695
Author(s):  
Philip Keith ◽  
Lauren Eyadiel ◽  
Jeremy Hodges ◽  
Karen Sands ◽  
Jared Watkins

2020 ◽  
Author(s):  
Steven P LaRosa ◽  
Steven M. Opal

Sepsis, along with the multiorgan failure that often accompanies this condition, is a leading cause of mortality in the intensive care unit. Although modest improvements in the prognosis have been made over the past two decades and promising new therapies continue to be investigated, innovations in the management of septic shock are still required. This chapter discusses the definitions, epidemiology, and pathogenesis (including microbial factors, host-derived mediators, and organ dysfunction) relating to sepsis. Management of severe sepsis and septic shock is also described.  This review contains 5 figures, 11 tables, and 99 references. Keywords:Organ dysfunction, sepsis, septic shock, infection, bacteremia, fluid resuscitation, vasopressor


CHEST Journal ◽  
2015 ◽  
Vol 148 (4) ◽  
pp. 190A
Author(s):  
Bravein Amalakuhan ◽  
Sheila Habib ◽  
Mandeep Mangat ◽  
Reyes Luis ◽  
Antonio Anzueto ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Quentin Maestraggi ◽  
Benjamin Lebas ◽  
Raphaël Clere-Jehl ◽  
Pierre-Olivier Ludes ◽  
Thiên-Nga Chamaraux-Tran ◽  
...  

Fundamental events driving the pathological processes of septic shock-induced multiorgan failure (MOF) at the cellular and subcellular levels remain debated. Emerging data implicate mitochondrial dysfunction as a critical factor in the pathogenesis of sepsis-associated MOF. If macrocirculatory and microcirculatory dysfunctions undoubtedly participate in organ dysfunction at the early stage of septic shock, an intrinsic bioenergetic failure, sometimes called “cytopathic hypoxia,” perpetuates cellular dysfunction. Short-term failure of vital organs immediately threatens patient survival but long-term recovery is also severely hindered by persistent dysfunction of organs traditionally described as nonvital, such as skeletal muscle and peripheral blood mononuclear cells (PBMCs). In this review, we will stress how and why a persistent mitochondrial dysfunction in skeletal muscles and PBMC could impair survival in patients who overcome the first acute phase of their septic episode. First, muscle wasting protracts weaning from mechanical ventilation, increases the risk of mechanical ventilator-associated pneumonia, and creates a state of ICU-acquired muscle weakness, compelling the patient to bed. Second, failure of the immune system (“immunoparalysis”) translates into its inability to clear infectious foci and predisposes the patient to recurrent nosocomial infections. We will finally emphasize how mitochondrial-targeted therapies could represent a realistic strategy to promote long-term recovery after sepsis.


2020 ◽  
Author(s):  
Steven P LaRosa ◽  
Steven M. Opal

Sepsis, along with the multiorgan failure that often accompanies this condition, is a leading cause of mortality in the intensive care unit. Although modest improvements in the prognosis have been made over the past two decades and promising new therapies continue to be investigated, innovations in the management of septic shock are still required. This chapter discusses the definitions, epidemiology, and pathogenesis (including microbial factors, host-derived mediators, and organ dysfunction) relating to sepsis. Management of severe sepsis and septic shock is also described.  This review contains 5 figures, 11 tables, and 99 references. Keywords:Organ dysfunction, sepsis, septic shock, infection, bacteremia, fluid resuscitation, vasopressor


2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Peter A. Ward ◽  
Ren-Feng Guo ◽  
Niels C. Riedemann

There is evidence in sepsis, both in rodents and in humans, that activation of the complement system results in excessive production of C5a, which triggers a series of events leading to septic shock, multiorgan failure, and lethality. In rodents following cecal ligation and puncture (CLP), which induces polymicrobial sepsis, in vivo blockade of C5a using neutralizing antibodies dramatically improved survival, reduced apoptosis of lymphoid cells, and attenuated the ensuing coagulopathy. Based on these data, it seems reasonable to consider therapeutic blockade of C5a in humans entering into sepsis and septic shock. Strategies for the development of such an antibody for use in humans are presented.


Critical Care ◽  
2010 ◽  
Vol 14 (Suppl 1) ◽  
pp. P506
Author(s):  
M Soliman ◽  
A Battah ◽  
H Elsherif ◽  
A Elsherif ◽  
H Khaled Nagi

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