Debriding action

There are many reports that wounds dressed with honey are rapidly debrided to give a clean granulating wound bed (Cavanagh et al, 1970; Armon, 1980; Braniki, 1981; Efem, 1993; Subrahmanyam, 1998; Dunford et al, 2000b; Alcaraz and Kelly, 2002; Ahmed et al, 2003), slough and necrotic tissue painlessly lifting off (Subrahmanyam, 1991; Efem, 1993; Subrahmanyam, 1993; Hejase et al, 1996; Subrahmanyam, 1996). Although induction of autolytic debridement is a feature of all wound dressings that give a moist environment, the debriding action of honey is faster than with other dressings and, on sloughy wounds, is about as rapid as that experienced using maggots (Julie Betts, Waikato Hospital: personal communication). Where there is hard eschar, maggot therapy provides a faster method of debridement as the maggots appear to burrow under the edges of the eschar, but honey dressings will remove hard eschar, especially if this is scored to aid penetration of the honey, and if the honey is diluted with water or saline so that it softens the eschar. Furthermore, using honey instead of maggots, removes the problems of obtaining a supply of freshly prepared material, of ensuring that the wound is not too wet (causing drowning) or too dry (killing by dehydration), or of keeping the maggots in place, and of overcoming patients’ unease with the squirming movement of the maggots.

The debriding action of maggots is due to the proteolytic enzyme activity they secrete, but with honey there does not appear to be a direct proteolytic activity involved: the existence of protein-digesting enzyme activity in honey has not been reported. Therefore, there must be a mechanism by which honey activates dormant proteolytic enzyme activity within the wound tissue, but in a controlled way so as not to cause unwanted digestion of the tissue. There is a strong association between high protease activity and impaired wound healing, and dressings are now being produced that inhibit or bind up and inactivate excessive protease activity in wounds that would otherwise be digesting wound tissue (Edwards et al, 2001; Cullen et al, 2002; Edwards et al, 2004). As mentioned earlier, the tissue-digesting collagenase and elastase enzyme activity in wounds is activated by oxidation. The antioxidant activity of honey can be expected to suppress this, just as the anti-inflammatory activity suppresses the infiltration of elastase-secreting neutrophils. This decreases the amount of enzyme released and, subsequently, the activity of that enzyme. The most likely explanation of the debriding activity induced by honey is that it promotes conversion of inactive plasminogen in the wound matrix to the active form, plasmin. This is an enzyme that functions to break down fibrin clots which attach slough and eschar to the wound bed. This action of honey could also be attributed to its anti-inflammatory activity, as inflammation causes inhibition of fibrinolysis by elevating the level of PAl-1 (plasminogen activator inhibitor 1) and thus preventing plasminogen from being converted to the active enzyme plasmin (Esmon, 2004). Fibrin is very common in chronic wounds (Schultz et al, 2003). (The enzyme streptokinase that is often used to debride wounds functions by activating plasminogen.)

The osmotic action of honey may also assist, as drawing out lymph from the wound tissues gives a constantly replenished supply of plasminogen at the interface of the wound bed and the overlying slough. Another advantage of this osmotic action of honey is that it washes the surface of the wound bed from beneath. This would account for the long-known feature of honey dressings to remove dirt with the dressing (Zaiß, 1934), making such dressings an excellent way of cleaning up grazes in which grit has become embedded.

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