[1][2] It is one of four categories of shock, a condition where there is not enough oxygen-carrying blood to meet the metabolic needs of the cells which make up the body's tissues and organs.
[1] Elbers and Ince have identified five classes of abnormal microcirculatory flow in distributive shock using side stream dark field microscopy.
[5] The endothelial cells lining the blood vessels become less responsive to vasoconstrictive agents, lose their glycocalyx (normal coating) and negative ionic charge, become leaky and cause extensive over-expression of nitric oxide.
[4] Tissue factor that initiates the clotting cascade is produced by activated monocytes and the endothelial cells lining the blood vessels while antithrombin and fibrinolysis are impaired.
[4] The ability of red blood cells to change shape decreases and their tendency to clump together increases, inhibiting their flow through the microvasculature.
This happens due to the widespread peritoneal irritation by the ruptured viscus contents, as in peptic ulcer perforation, with consequent strong vagal activation, and generalized, extensive peripheral vasodilation and bradycardia.
[2] Control of inflammation, vascular function and coagulation to correct pathological differences in blood flow and microvascular shunting has been pointed to as a potentially important adjunct goal in the treatment of distributive shock.