The pathogenesis of septic shock and MODS derives from mediators produced because of the immune response of the host. Despite encouraging data from animal studies, immunosuppressive agents, such as high-dose corticosteroids, have not shown any benefit in humans.
The Surviving Sepsis Campaign recommends that glucose levels in the septic patient should be kept at less than 150 mg/dL.
Research has focused on modifying the host response to sepsis via a number of approaches, including the following:
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Antibodies against gram-negative endotoxin
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Gamma globulins
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Monoclonal antibodies against tumor necrosis factor
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Blockade of eicosanoid production
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Blockade of interleukin (IL)–1 activity
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Inhibition of nitric oxide (NO) synthase
These approaches have met with modest success in animal experiments, but at present, they cannot be recommended for general use in humans.
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Stages of sepsis based on American College of Chest Physicians/Society of Critical Care Medicine Consensus Panel guidelines.
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Pathogenesis of sepsis and multiorgan failure.
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Venn diagram showing overlap of infection, bacteremia, sepsis, systemic inflammatory response syndrome (SIRS), and multiorgan dysfunction.
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Acute respiratory distress syndrome (ARDS) present in this chest x-ray (CXR) film is a common organ system affected in multiorgan failure of sepsis.
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Acute respiratory distress syndrome (ARDS) shown in this chest x-ray (CXR) film is a common complication of septic shock. Note bilateral airspace infiltration, absence of cardiomegaly, vascular redistribution, and Kerley B lines.
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Organizing phase of diffuse alveolar damage (ARDS) secondary to septic shock shows diffuse alveolar injury and infiltration with inflammatory cells.
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Organizing diffuse alveolar damage in a different location showing disorganization of pulmonary architecture.
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A high-power view of organizing diffuse alveolar damage (ARDS) shows hyperplasia of type II pneumocytes and hyaline membrane deposits.
