Sepsis severa y choque septico

Notas del editor

• #5: As long ago as 2735 B.C., the Chinese Emperor, Sheng Nung, wrote about the use of herbal medicines to treat fever brought on by sepsis. La reseña más antigua que tenemos de sepsis asociada a heridas se remonta al papiro descubierto por Edwin Smith en 1862 en las afueras de Luxor, Egipto.3 Redactado cerca de 1600 a. C., este papiro parece ser la copia de otro manuscrito muy anterior que data del año 3000 a. C., por lo cual se lo considera el tratado de cirugía más antiguo que se conoce.4,5 En él se hace referencia a 48 casos de lesiones traumáticas entre heridas, fracturas y luxaciones en diversas partes del cuerpo explicando sus síntomas y signos así como su seguimiento, pronóstico y tratamiento The concept of anti-sepsis (an organized, rational effort to prevent and treat sepsis) was originated by John Pringle, Surgeon General of the British army in the 18th century. A century later, Ignaz Semmelweis introduced antiseptic techniques for the care of women during childbirth. Semmelweis's advances brought the death rate from puerperal fever down from 13.6% of all women who were giving birth to 1.5%. In 1879, the French physician Louis Pasteur identified the streptococcus bacteria as the cause of puerperal sepsis.
• #9: Binding = Ligar TLR 4 = Toll Like Receptor 4 Activador del sistema inmune por bacterias TLR 2 = Toll Like Receptor 2 Activador del sistema inmune por toxinas y bacterias El NF-kB (factor nuclear potenciador de las cadenas ligeras kappa de las células B activadas) es un complejo proteico que controla la transcripción del ADN
• #19: El PAI-1 (inhibidor del activador del plasminógeno-1) es el principal inhibidor del activador tisular del plasminógeno (t-PA) y la uroquinasa (uPA), los activadores del plasminógeno y por lo tanto de la fibrinolisis (la eliminación fisiológica de los trombos de la sangre). EPCR Receptor activador de proteina C T-PA Activador tisular del plasminogeno
• #26: Adequate fluid resuscitation is defined as infusion of 20 to 30 mL/kg of starch, infusion of 40 to 60 mL/kg of saline solution, or a measured pulmonary capillary wedge pressure (PCWP, also known as the pulmonary artery occlusion pressure) of 12 to 20 mmHg. For patients who have a central venous catheter rather than a pulmonary arterial catheter, a central venous pressure (CVP) of 8 to 12 mmHg is a reasonable substitute.
• #27:  Refractory septic shock exists if maintaining the systemic mean blood pressure >60 mmHg (or >80 mmHg if the patient has baseline hypertension) requires dopamine >15 mcg/kg per min, norepinephrine >0.25 mcg/kg per min, or epinephrine >0.25 mcg/kg per min despite adequate fluid resuscitation. Adequate fluid resuscitation is defined as infusion of 20 to 30 mL/kg of starch, infusion of 40 to 60 mL/kg of saline solution, or a measured pulmonary capillary wedge pressure (PCWP, also known as the pulmonary artery occlusion pressure) of 12 to 20 mmHg. 
• #36: ● Broad-spectrum: one or more agents active against likely bacterial/fungal pathogens and with good penetration into presumed source (1B) ● Reassess antimicrobial regimen daily to optimize efficacy, prevent resistance, avoid toxicity, and minimize costs (1C) Consider combination therapy in Pseudomonas infections (2D) Consider combination empiric therapy in neutropenic patients (2D) Combination therapy 3–5 days and de-escalation following susceptibilities (2D) ● Duration of therapy typically limited to 7–10 days; longer if response is slow or there are undrainable foci of infection or immunologic deficiencies (1D) ● Stop antimicrobial therapy if cause is found to be noninfectious (1D)
• #65: ○ Critically ill patients: Insulin therapy should be initiated for treatment of persistent hyperglycemia starting at a threshold of no greater than 180 mg/dL (10 mmol/L). Once insulin therapy is started, a glucose range of 140–180 mg/dL (7.8 to 10 mmol/L) is recommended for the majority of critically ill patients. (A) ○ More stringent goals, such as 110–140 mg/dL (6.1–7.8 mmol/L) may be appropriate for selected patients, as long as this can be achieved without significant hypoglycemia. (C) ○ Critically ill patients require an intravenous insulin protocol that has demonstrated efficacy and safety in achieving the desired glucose range without increasing risk for severe hypoglycemia.