Antibiotics are ineffective in penetrating chronic, nonhealing wounds. Debridement is the greatest option for clearing bacterial loads and removing nonviable tissue. Otherwise performed, necrotic material can release endotoxins that inhibit keratinocyte migration and matrix production, and may prolong the inflammatory response, promoting matrix-destroying proteases. Methods of debridement include sharp, mechanical, chemical and biodebridement.
Sharp, or surgical debridement affords the luxury of speed, because it can be performed in the bedside without a penny more than scissors and two forceps. More extensive debridement may require anesthesia, and should be performed in the operating room.
Mechanical debridement is the eradication of dead tissue by the sequential changes of dressings that are inserted moist into the wound and removed after they can dry. Exudative and necrotic tissues stick to the drying gauze and therefore are brought out from the wound with the gauze. This method only has a limited ability to remove structurally intact or strongly adherent devitalized tissue. The classic "wet-to-dry" dressing is really a mechanically debriding dressing.
Chemical debriding agents are enzymatic compounds that break up tissue. They're best in moderately sized regions of necrosis or in those patients that will not tolerate an operation. In order to achieve maximum benefit, larger eschars should be cross-hatched or excised to permit for better penetration of the agent. The papain-containing cream, Accuzyme, is commonly used for this purpose. Biodebridement requires the application of sterile maggots into a wound for periods of 48-72 hours. The maggots feast upon, and therefore remove dead tissue before being irrigated out. This method could be repeated as necessary. Needless to say, it's not a commonly used technique.
Antibiotics do have a job in the treatment of chronic, infected wounds once debridement has achieved healthy wound borders. Empiric antibiotics should be selected based on the bacteria that are likely to be involved. For example, empiric antibiotics for wounds near the oropharynx and diabetic foot wounds should include coverage for anaerobic species.
The Gram stain can provide a general concept of whether Gram-positive, Gram-negative or a combination of bacteria is present. Once culture results return over the subsequent 2-3 days, antibiotic coverage should be tailored to the involved organisms. Topical antibiotic preparations can help to lessen bacterial load and may be used with a few success in an adjuvant setting in the select wound population. Prudence should be taken using their use, however, because many of these preparations also impair the function from the superficial cells necessary for wound healing. They should never be used in wounds associated with venous disease, because these wounds are more vulnerable to sensitivity reactions.
These include: iodine or iodophor paint, sodium hypochlorite solution, hydrogen peroxide, acetic acid, antibiotic creams or even the newer cadhexomer iodine and nanocrystalline silver. For wounds that arise in the setting of underlying pathology, treating the condition process can increase the speed and likelihood of wound healing. For venous stasis ulcers, reducing edema fluid with Unna boot compression, elevation and diuresis can improve oxygen delivery and thus cellular function.
Patients with diabetic foot ulcers must have their blood sugar strictly controlled given the deleterious effects of hyperglycemia on neutrophil and monocyte function. If ischemia is thought to be contributing to the etiology or chronicity of a wound, smoking cessation and elimination of dehydration and anemia should all be considered in the treatment plan. Ultimately arterial revascularization with or without surgical reconstruction using local or microvascular flaps might be necessary.
This problem is a result of infection from the apocrine sweat glands, most often in the axillary, perineal and groin regions. It results in recurrent, draining abscesses and sinus tracts that can result in severe pain and debilitation.
Lesions in the axilla that heal may scar and secondarily cause contracture limiting arm motion. Active infection should be treated with a 1-2 week span of oral antibiotics and it is usually due to Gam positive cocci. Cultures ought to always be taken since other bacterial infections may appear, and also the antibiotic should be appropriately selected.
Surgical treatment consists of full-thickness excision from the infected dermis and any involved fat under the skin. Primary closure can be obtained in small- to moderate-sized wounds without active infection. Larger defects, or those that are grossly infected, should not be closed primarily.
They should be permitted to granulate with dressing changes, then split-thickness skin grafting or healing by secondary intention. Incomplete excision of the involved tissue is typical because of retained sinus tracts or deep infected glands. If this occurs, there's a high probability of recurrence and skin graft failure.
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