Acute inflammation typically occurs before the immune response becomes

established and aims primarily at removing the injury causing agent and limiting the
extent of tissue damage. Acute inflammation occurs in two overlapping stages,
vascular and cellular. In the vascular stage, arterioles and venules near the site of
injury constrict briefly then dilate. Dilation promotes congestion, while an
accompanying increase in capillary permeability leads to the movement of fluid into
the affected tissue, resulting in the 5 cardinal signs of inflammation. As fluid leaves
the capillaries, the blood remaining in circulation becomes more viscous, and clotting
occurs. The cellular stage of acute inflammation is initiated by the movement of
phagocytic white blood cells or leukocytes into the area of injury. The leukocytes
begin to adhere to the vessel wall and then in a process called emigration, squeeze
through the wall and move into the inflamed tissue. The leukocytes wander into the
tissue guided by chemical signals in a process called chemotaxis. The cellular stage
ends in the leukocytes engulfing and degrading the bacteria and cellular debris in a
process called phagocytosis. Products of phagocytosis along with plasma and blood
cells form exudates, which accumulate and cause swelling and pain. Exudates are
composed of serous fluid and red blood cells, fibrinogen or tissue debris and white
blood cell break-down products. Concurrent with the events of the vascular and
cellular stages, chemical mediators release bioactive agents that act to mediate the
inflammatory response. Mediators are derived from the cells or from plasma. One of
the first mediators of an inflammatory response is a cell-derived mediator, histamine,
found in high concentrations in the mast cells of connective tissues adjacent to blood
vessels as well as in blood basophils and platelets. Histamine is released in response
to a variety of stimuli and causes dilation and increased permeability of capillaries.
Serotonin, another cell-derived mediator performs similar actions. The 3 major
plasma derived mediators are present in the plasma in precursor forms that must be
activated usually by a series of protiolytic enzymes. The kinins increase capillary
permeability and stimulate pain receptors. The clotting system (fibrin strands) traps
exudates, microorganisms and foreign bodies. The complement cascade causes
vasodilation, promotes leukocyte chemotaxis and enhances phagocytosis.