Can you explain the connection between septicaemia and septic shock / disseminated intravascular coagulation (DIC)?
This applies particularly to septicaemia with Gram negative bacteria. The lipopolysaccharide component of their cell wall has ENDOTOXIN activity and activates a range of host cells/systems to release chemical mediators with wide ranging biological activity. One of the consequences of this cascade is increased capillary permeability that leads to loss of fluid and decreased blood volume. This is referred to as hypovolaemic shock. Another consequence of the intravascular release of endotoxin is that it stimulates intravascular clotting. In a simplified explanation, imagine that as you start clotting within the blood vessels, small fragments of clots break off (emboli) and eventually become lodged in small capillaries and block the supply of blood to tissues distal to the site of the lodged clot. This is leads to infarction of those tissues, and this is why many people that suffer endotoxic shock during meningococcal infection end up with fingers or toes being amputated. Since you only ha
