Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
-
Early fluid administration is fundamental for the initial treatment of severe sepsis and septic shock patients. A large portion of suspected severe sepsis and septic shock patients can be quickly resuscitated with therapeutic tests until surrogate cardiac output markers, such as heart rate and urinary output, are normalized. ⋯ When clinical stabilization is not achieved with initial fluid resuscitation, more careful, complete, and accurate monitoring should be started for both reversing tissue hypoxia and preventing fluid overload. This challenge requires appropriate knowledge of the physiological foundations governing the different monitoring method advantages and their respective limitations, therefore allowing the election of the best therapeutic measures for each different scenario.
-
Leptospirosis is an acute septicemic illness that affects humans in all parts of the world. Approximately 10% of patients with leptospirosis develop severe disease, the Weil syndrome, with jaundice, acute kidney injury (AKI), and pulmonary hemorrhage. Leptospirosis-induced AKI is typically nonoliguric with a high frequency of hypokalemia. ⋯ Studies with hamsters demonstrated that in leptospirosis a noncardiogenic pulmonary edema occurs consequently to a decrease in the clearance of alveolar fluid, due to a decrease in sodium transporter in the luminal membrane (ENaC) and an increase in the NKCC1 basolateral membrane transporter. Antibiotic treatment is efficient in the early and late/severe phases and revert all kidney transporters. Early and daily hemodialysis, low daily net fluid intake, and lung-protective strategies are recommended for critically ill patients with leptospirosis.
-
Acute coagulopathy of trauma (aCOT) is a state of disordered coagulation developing soon after severe injury and blood loss and has been defined in the clinical literature as an elevation in prothrombin time (PT) and activated partial thromboplastin time (aPTT). ⋯ This model of aCOT in rats showed complex changes in clotting parameters over 4 h that included a rise in PT and aPTT. At 4 h, there was a decrease in clotting firmness, even though the clot formation was faster (elevated α angle and decrease in clotting time). The decrease in clotting firmness correlated with falling fibrinogen and platelet count. This model affords an opportunity to evaluate interventions in the treatment of aCOT.
-
Inflammation is powerful response to destroy invading organisms, and an exaggerated response can lead to death of the host. Macrophages secrete mediators that activated circulating neutrophils leading to its migration into infectious site. Recently, it has been shown that lymphocytes have an action modulating the early phase of inflammatory response. ⋯ On the other hand, B1 cells are shown to be detrimental in other mouse models of microbial infection, such as experimental Chagas disease, leishmaniasis, and Staphylococcus aureus-induced arthritis. B1 cell plays a protective role in the host of the effects of endotoxemia. In a murine model of endotoxemia by lipopolysaccharide, B1 cell participates in both interleukin 10 and immunoglobulin M secretion with a consequent reduction in mortality.
-
Sepsis is a major cause of mortality and morbidity in intensive care units. Acute and long-term brain dysfunctions have been demonstrated both in experimental models and septic patients. ⋯ The mechanisms of sepsis-associated encephalopathy involve mitochondrial and vascular dysfunctions, oxidative stress, neurotransmission disturbances, inflammation, and cell death. Here we review specific evidence that links bioenergetics, mitochondrial dysfunction, and oxidative stress in the setting of brain dysfunctions associated to sepsis.