Acute Inflammation Clinical Picture

The five cardinal signs of acute inflammation are: redness, hotness, swelling, pain, and loss of function.

The purpose of the vascular changes is to dilute the toxins in the inflamed part and to supply more blood that contains leukocytes and antibodies to the area.

The increased volume in the dilated vessels leads to an increase in local hydrostatic pressure, which then causes transudation of protein-poor fluid into the extravascular space.

The two mechanisms are: i) Liberation of chemical mediators (e.g. histamine, kinin) which act directly on the muscle of the arterioles, and ii) Action of toxins and metabolites on arterioles.

The systemic manifestations of acute inflammation that may or may not be present include: a) Fever, malaise, loss of appetite and weight, b) Leukocytosis (increased leukocyte count to > 12,000/cmm), and c) Changes in plasma protein levels.

Increased vascular permeability of the microvasculature (vascular leakage), leading to the pouring of protein-rich fluid (exudate) into the extravascular tissues.

1. Leukocytes fall out of the central axial stream towards the endothelial lining (margination). 2) Leukocytes stick to the endothelium (adhesion). 3) Leukocytes migrate through the vascular wall into the interstitial tissue (extravasation).

The net result is fluid accumulation in interstitial tissues (inflammatory edema), which participates in swelling that is visible to the naked eye.

1. Direct endothelial injury: leading to endothelial cell necrosis and detachment. 2) Leukocyte-dependent endothelial injury: occurs due to the release of toxic oxygen species and proteolytic enzymes from leukocytes.

Exudates have a high protein content (> 1 gm%), containing different plasma proteins including fibrinogen, have a tendency to coagulate, and have a specific gravity > 1020. Transudates have a low protein content (< 1 gm%), containing mostly small proteins like albumin, have no tendency to coagulate, and have a lower specific gravity.