Critical care : the official journal of the Critical Care Forum
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This review examines experimental evidence that the microvascular dysfunction that occurs early in sepsis is the critical first stage in tissue hypoxia and organ failure. A functional microvasculature maintains tissue oxygenation despite limitations on oxygen delivery from blood to tissue imposed by diffusion; the density of perfused (functional) capillaries is high enough to ensure appropriate diffusion distances, and arterioles regulate the distribution of oxygen within the organ precisely to where it is needed. ⋯ However, within hours of the onset of sepsis, a dysfunctional microcirculation is, due to a loss of functional capillary density and impaired regulation of oxygen delivery, unable to maintain capillary oxygen saturation levels and prevent the rapid onset of tissue hypoxia despite adequate oxygen supply to the organ. The mechanism(s) responsible for this dysfunctional microvasculature must be understood in order to develop appropriate management strategies for sepsis.
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Comparative Study Clinical Trial
Circulating immune parameters predicting the progression from hospital-acquired pneumonia to septic shock in surgical patients.
Hospital-acquired pneumonia after surgery is one of the major causes of septic shock. The excessive inflammatory response appears to be responsible for the increased susceptibility to infections and subsequent sepsis. The primary aim of this study was to investigate immune parameters at the onset of pneumonia, before the development of subsequent septic shock. The secondary aim was to investigate the usefulness of these immune parameters in predicting progression from hospital-acquired pneumonia to septic shock. ⋯ At the onset of hospital-acquired pneumonia, a significant relevant systemic cytokine mediated response had already been initiated. It might, therefore, be possible to identify patients at risk for septic shock with these predictive markers during early pneumonia. In addition, immune modulating therapy might be considered as adjuvant therapy.
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Reduced microvascular perfusion has been implicated in organ dysfunction and multiple organ failure associated with severe sepsis. The precise mechanisms underlying microvascular dysfunction remain unclear, but there are considerable experimental data showing reduced microcirculatory flow, particularly of small vessels, and increased heterogeneity. ⋯ Importantly, the degree of microvascular disturbance and its persistence is associated with poorer outcomes. The ability to influence these changes may result in better outcomes and bedside systems, enabling direct visualization of the microcirculation, which will help in the assessment of ongoing microcirculatory dysfunction and its response to established and new therapeutic interventions.
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Experimental and clinical studies have shown a reduction in intrapulmonary shunt with spontaneous breathing during airway pressure release ventilation (APRV) in acute lung injury. This reduction was related to reduced atelectasis and increased aeration. We hypothesized that spontaneous breathing will result in better ventilation and aeration of dependent lung areas and in less cyclic collapse during the tidal breath. ⋯ Spontaneous breathing during APRV redistributes ventilation and aeration to dependent, usually well-perfused, lung regions close to the diaphragm, and may thereby contribute to improved arterial oxygenation. Spontaneous breathing also counters cyclic collapse, which is a risk factor for ventilation-associated lung injury.
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The authors of a recent paper have described an updated simplified acute physiology score (SAPS) II mortality model developed on patient data from 1998 to 1999. Hospital mortality models have a limited range of applicability. SAPS II, Acute Physiology, Age, and Chronic Health Evaluation (APACHE) III, and mortality probability model (MPM)-II, which were developed in the early 1990s, have shown a decline in predictive accuracy as the models age. ⋯ In particular, mortality tends to get over predicted when older models are applied to more contemporary data, which in turn leads to 'grade inflation' when benchmarking intensive care unit (ICU) performance. Although the authors claim that their updated SAPS II can be used for benchmarking ICU performance, it seems likely that this model might already be out of calibration for patient data collected in 2005 and beyond. Thus, the updated SAPS II model may be interesting for historical purposes, but it is doubtful that it can be an accurate tool for benchmarking data from contemporary populations.