WHAT ARE SEPSIS AND SEPTIC SHOCK?

WHAT ARE SEPSIS AND SEPTIC SHOCK?

  1. 1
    WHAT IS THE MEANING OF SEPSIS AND SEPTIC SHOCK?
    • The definitions of terms related to sepsis are given in Table 1–1. Physiologically similar systemic inflammatory response syndrome can be seen even in the absence of identifiable infection.

    (CI, cardiac index; HR, heart rate; INR, international normalised ratio; RR, respiratory rate; SD, standard deviation; SIRS, systemic inflammatory response syndrome; T, temperature; WBC, white blood cell (count).)

    Adapted from Levy MM, Fink MP, Marshall JC, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med 2003; 31:1250-1256.

  2. 2
    WHAT ARE THE CAUSES OF SEPSIS AND SEPTIC SHOCK?
    • The sites of infections that most frequently lead to sepsis are the respiratory tract (39%–50%), urinary tract (5%–37%), and intra-abdominal space (8%–16%). Sepsis may be caused by gram-negative (50%–62% of sepsis) or gram-positive bacteria (37%–47%), as well as by fungi (5%) or other microorganisms.
    • Escherichia coli, Klebsiella species, and Pseudomonas aeruginosa are the most commonly isolated gram-negative pathogens in sepsis. Other common gram-negative pathogens are Serratia spp., Enterobacter spp., and Proteus spp. P. aeruginosa is the most frequent cause of sepsis fatality. Common gram-positive pathogens are Staphylococcus aureus, Streptococcus pneumoniae, coagulase-negative staphylococci, and Enterococcus species.
    • Candida species (particularly Candida albicans) are common fungal etiologic agents of bloodstream infections. The 30-day mortality rate for sepsis due to candidemia was 54%.
    • The pathophysiologic focus of gram-negative sepsis has been on the lipopolysaccharide (endotoxin) component of the gram-negative cell wall. Lipid A is a part of the endotoxin molecule from the gram-negative bacterial cell wall that is highly immunoreactive and is responsible for most of the toxic effects.
    • Sepsis involves a complex interaction of proinflammatory (e.g., tumour necrosis factor-α [TNF-α]; interleukin [IL]-1, IL-6) and anti-inflammatory mediators (e.g., IL-1 receptor antagonist, IL-4, and IL-10). IL-8, platelet- activating factor, leukotrienes, and thromboxane A2 are also important.
    • TNF-α is considered the primary mediator of sepsis. Concentrations are elevated early in the inflammatory response during sepsis, and there is a correlation with the severity of sepsis. TNF-α release leads to activation of other cytokines associated with cellular damage, and it stimulates the release of arachidonic acid metabolites that contribute to endothelial cell damage. A primary mechanism of injury with sepsis is through endothelial cells. With inflammation,   endothelial cells allow  circulating cells (e.g., granulocytes) and plasma constituents to enter inflamed tissues, which may result in organ damage.
    • A key endogenous substance involved in the inflammation of sepsis is activated protein C, which enhances fibrinolysis and inhibits inflammation. Levels of protein C are reduced in patients with sepsis.
    • Shock is the most ominous complication associated with gram-negative sepsis and causes death in about one-half of patients. Another complication is disseminated intravascular coagulation (DIC), which occurs in up to 50% of patients with septic shock. DIC is the inappropriate activation of the clotting cascade that causes the formation of microthrombi, resulting in the consumption of coagulation factors, organ dysfunction, and bleeding. Acute respiratory distress syndrome (ARDS) is another common complication of sepsis.
    • The hallmark of the hemodynamic effect of sepsis is the hyperdynamic state characterised by high cardiac output and an abnormally low systemic vascular resistance.
KNOWLEDGE BASE
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