Endotoxin release from meningococcal bacteraemia results in increased vascular permeability, with the passage of protein and water from the intravascular to the extravascular space. This effect is mediated by an inflammatory response targeted at the endothelial lining of the blood vessels. This capillary leak syndrome causes a reduction in circulating volume, hypovolaemia, and a reduction in cardiac output.

Acute myocardial dysfunction contributes to the picture of septic shock in meningococcal septicaemia. Meningococcal endotoxin and other associated inflammatory mediators have a direct myocardial depressant effect and this, in combination with a myocardial cytotoxic effect, can cause myocardial cell necrosis.

DIC is a recognised sequelae of IMD, resulting from activation of the coagulation cascade, and down regulation of the anticoagulant and fibrinolytic pathways, leading to a pro-coagulant state. This process explains the characteristic petechial and purpuric rash associated with meningococcal septicaemia.

The progression of shock results in tissue hypoxia and pulmonary oedema from capillary leak. When decompensation occurs, hypotension results, which is a pre-terminal sign in children with meningococcal septicaemia.