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Acute wound exudate contains molecules and cells that are vital to support the healing process.
It has a high protein content (although lower than that found in serum), with a specific gravity greater than 1.020.
In chronic wounds, the colour, consistency and amount of exudate may change as a result of various physiological processes  See Table 2. Some strains of Staphylococcus aureus, β-haemolytic group A streptococci and Bacteroides fragilis, produce fibrinolysins. This has been attributed in part to specific bacterial virulence mechanisms that result in vasodilation and extravasation .
Pseudomonas aeruginosa produces a non-specific enzyme that degrades fibrin. Gautam et al (2001)  have described a process whereby neutrophils attracted to the site of injury trigger the release of heparin-binding protein (HBP).
Certain bacteria such as Pseudomonas aeruginosa stimulate the release of HBP from neutrophils, thus aggravating chronic inflammation by augmenting endothelial hyper-permeability .
It is likely that HBPs are implicated in the production of increased exudate.
Its composition includes electrolytes, glucose, cytokines, leukocytes, metalloproteinases, macrophages and micro-organisms .
In the first 48 to 72 hours after wounding, platelets and fibrin may be present, but this reduces as bleeding diminishes. As fluid passes through the inflamed vessel walls (extravasation) it may be seen that wound exudate is in essence modified serum and will therefore contain similar solutes.
Exudate management is relevant to patient quality-of-life issues as it is often associated with leakage and malodour.
It impacts on health economics because failure to control exudate production will lead to increased management costs and patient morbidity.