Septic shock is an inflammatory condition which results from a cascade of pro-inflammatory events mediated by molecules such as Cytokines e.g. tumor necrosis factor (TNS). The definition of shock is when arterial pressure is too low to maintain an adequate profusion of blood to tissues. In the case of septic shock there is a dramatic decrease in the volume of blood circulating in the arteries because the capillaries have dilated and there is endothelial damage resulting in blood leaking from the vessels into extravascular compartments.
Many complications can arise from septic shock due to the hypotension caused by the leaking capillaries. Even if the initial causative agent of septic shock is treated a patient may still die from the effects of septic shock, for example acute tubular necrosis (ATN) can result if the very high and specific blood demand of the kidneys is not met. This can lead to kidney failure which a patient may die from.
Septic shock is the second biggest killer in adult intensive care units (the biggest is Cardiogenic problems). Clinical features are: a weak rapid pulse, irregular breathing, cold sweaty pale skin, dilated pupils, fever, hypotension and disseminated intravascular coagulation (DIC), which is caused by activation of blood coagulation by endothelial damage, endotoxins and immune complexes.
Septic shock is difficult to treat because of its rapid onset. The patient's condition worsens quickly. The causative agent must be identified very quickly and appropriately treated. There are new treatments on the horizon but they need more extensive trials before they can come into use.