Critical care clinics
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Sepsis results in many deaths, prolonged suffering among survivors and relatives, and high use of resources both in developed and developing countries. The updated Surviving Sepsis Campaign guidelines should aid clinicians in improving the identification and management of these patients, but many uncertainties remain because most of the guidance is based on low-quality evidence. This article discusses how to use some of the specific items of the guidelines together with a common-sense approach to aid clinical management of patients with sepsis while trying to balance the potential benefit and harm of the items.
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Sepsis is characterized by early massive catabolism, lean body mass (LBM) loss, and escalating hypermetabolism persisting for months to years. Early enteral nutrition should attempt to correct micronutrient/vitamin deficiencies, deliver adequate protein and moderated nonprotein calories, as well-nourished patients can generate reasonable endogenous energy. ⋯ Malnutrition screening is essential, and parenteral nutrition can be safely added when enteral nutrition is failing based on preillness malnutrition. Following discharge from intensive care unit, significantly increased protein/calorie delivery is required for months to years to facilitate functional and LBM recovery.
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Sepsis is caused by a dysregulated host response to infection. Immune responses determine the characteristics of sepsis. The body's protection against infection involves danger signal surveillance and recognition from nonself, effector functions in response to sensing danger signals, homeostatic regulation, and generation of immunologic memory. ⋯ Detecting these molecular patterns generates multisystem responses. Impaired organ function remote to the site of infection is the unifying feature. The processes by which an appropriate response to a microbial invader change from adaptive to maladaptive and dysregulated remain unclear.
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Sepsis describes a broad-based syndrome covering many infectious agents, affecting various sites in patients of differing age, gender, and comorbidity and resulting in varying degrees and combinations of organ dysfunction. Protocolized care with rigid goals may suit populations, assuming the evidence-lite recommendations are beneficial, but not necessarily individual patients. ⋯ Other than clinical heterogeneity, a range of biological signatures exist in sepsis, and these fluctuate over the disease course. Subsets of septic patients can display distinct biological signatures that may potentially be used to identify suitability for different treatments and titration to optimal effect.
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Sepsis-associated organ dysfunction involves multiple responses to inflammation, including endothelial and microvascular dysfunction, immune and autonomic dysregulation, and cellular metabolic reprogramming. The effect of targeting these mechanistic pathways on short- and long-term outcomes depends highly on the timing of therapeutic intervention. Furthermore, there is a need to understand the adaptive or maladaptive character of these mechanisms, to discover phase-specific biomarkers to guide therapy, and to conceptualize these mechanisms in terms of resistance and tolerance.