miércoles, 3 de enero de 2018

Sepsis



Diciembre 31, 2017. No. 2949
Hoy ha llegado a su fin 2017, un año con múltiples facetas, con cambios vitales para nuestra vida que sin duda alguna nos han impactado positivamente y al reflexionar sobre los logros obtenidos estaremos reforzando nuestras metas, modificando algunos proyectos de vida, y lo más importante; continuaremos forjando nuestra felicidad al parejo de nuestros seres queridos, nuestros conocimientos para beneficio de cada uno de nuestros pacientes y la plena satisfacción personal de ser médicos en toda la extensión de la palabra.
¡Felicidades por cada uno de esos logros personales!
Today, 2017 has come to an end. A year with many facets, with vital changes to our lives, that without a doubt, have positively impacted us, and reflecting on our achievements we will be reinforcing our goals, modifying some life projects, and most importantly; We will continue to forge our happiness on the same level as our loved ones, our knowledge for the benefit of each one of our patients, and the full personal satisfaction of being a doctor in every sense of the word.
Congratulations on each of those personal achievements!
 Hoje chegou ao fim de 2017, um ano com muitas facetas, com mudanças vitais na nossa vida que, sem dúvida, nos impactaram positivamente e refletindo sobre as conquistas, reforçaremos nossos objetivos, modificando alguns projetos de vida e, o mais importante ; Continuaremos a forjar a nossa felicidade ao mesmo nível dos nossos amados, o nosso conhecimento em benefício de cada um dos nossos pacientes e a total satisfação pessoal de ser um médico em todos os sentidos da palavra.
Parabéns por cada uma dessas conquistas pessoais!
Diabetes y sepsis: riesgo, recurrencia y ruina.
Diabetes and Sepsis: Risk, Recurrence, and Ruination.
Front Endocrinol (Lausanne). 2017 Oct 30;8:271. doi: 10.3389/fendo.2017.00271. eCollection 2017.
Abstract
Sepsis develops when an infection surpasses local tissue containment. A series of dysregulated physiological responses are generated, leading to organ dysfunction and a 10% mortality risk. When patients with sepsis demonstrate elevated serum lactates and require vasopressor therapy to maintain adequate blood pressure in the absence of hypovolemia, they are in septic shock with an in-hospital mortality rate >40%. Traditionally, it was thought that the complex interplay between inflammatory and anti-inflammatory responses led to sepsis-induced organ dysfunction and mortality. However, a closer examination of those who die long after sepsis subsides reveals that many initial survivors succumb to recurrent, nosocomial, and secondary infections. The comorbidly challenged, physiologically frail diabetic individuals suffer the highest infection rates. Recent reports suggest that even after clinical "recovery" from sepsis, persistent alterations in innate and adaptive immune responses exists resulting in chronic inflammation, immune suppression, and bacterial persistence. As sepsis-associated immune defects are associated with increased mortality long-term, a potential exists for immune modulatory therapy to improve patient outcomes. We propose that diabetes causes a functional immune deficiency that directly reduces immune cell function. As a result, patients display diminished bactericidal clearance, increased infectious complications, and protracted sepsis mortality. Considering the substantial expansion of the elderly and obese population, global adoption of a Western diet and lifestyle, and multidrug resistant bacterial emergence and persistence, diabetic mortality from sepsis is predicted to rise dramatically over the next two decades. A better understanding of the underlying diabetic-induced immune cell defects that persist following sepsis are crucial to identify potential therapeutic targets to bolster innate and adaptive immune function, prevent infectious complications, and provide more durable diabetic survival.
KEYWORDS: complications; diabetes; infections; resource utilization; sepsis; septic shock
Carga de líquido inicial para pacientes sépticos: ¿Se necesita algún límite de seguridad?
Early fluid loading for septic patients: Any safety limit needed?
Chin J Traumatol. 2017 Nov 8. pii: S1008-1275(16)30323-6. doi: 10.1016/j.cjtee.2017.06.005. [Epub ahead of print]
Abstract
Early adequate fluid loading was the corner stone of hemodynamic optimization for sepsis and septic shock. Meanwhile, recent recommended protocol for fluid resuscitation was increasingly debated on hemodynamic stability vs risk of overloading. In recent publications, it was found that a priority was often given to hemodynamic stability rather than organ function alternation in the early fluid resuscitation of sepsis. However, no safety limits were used at all in most of these reports. In this article, the rationality and safety of early aggressive fluid loading for septic patients were discussed. It was concluded that early aggressive fluid loading improved hemodynamics transitorily, but was probably traded off with a follow-up organ function impairment, such as worsening oxygenation by reduction of lung aeration, in a part of septic patients at least. Thus, a safeguard is needed against unnecessary excessive fluids in early aggressive fluid loading for septic patients.
KEYWORDS: Fluid loading; Hemodynamic stability; Safety; Sepsis
Miocardiopatía inducida por sepsis: Implicaciones oxidativas en la iniciación y resolución del daño.
Sepsis-Induced Cardiomyopathy: Oxidative Implications in the Initiation and Resolution of the Damage.
Oxid Med Cell Longev. 2017;2017:7393525. doi: 10.1155/2017/7393525. Epub 2017 Sep 19.Abstract
Cardiac dysfunction may complicate the course of severe sepsis and septic shock with significant implications for patient's survival. The basic pathophysiologic mechanisms leading to septic cardiomyopathy have not been fully clarified until now. Disease-specific treatment is lacking, and care is still based on supportive modalities. Septic state causes destruction of redox balance in many cell types, cardiomyocytes included. The production of reactive oxygen and nitrogen species is increased, and natural antioxidant systems fail to counterbalance the overwhelming generation of free radicals. Reactive species interfere with many basic cell functions, mainly through destruction of protein, lipid, and nucleic acid integrity, compromising enzyme function, mitochondrial structure and performance, and intracellular signaling, all leading to cardiac contractile failure. Takotsubo cardiomyopathy may result from oxidative imbalance. This review will address the multiple aspects of cardiomyocyte bioenergetic failure in sepsis and discuss potential therapeutic interventions.

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