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KEY POINTS
Chronic wounds are becoming an increasing problem among all races.
The basic biology of wound healing applies to skin of light and dark color.
Certain pathologic processes are more common in skin of color, such as keloids and postinflammatory hyperpigmentation.
Diversity in skin color can pose a challenge in assessing patients with wounds.
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Diversity in skin color can pose a challenge in assessing patients with wounds. For example, erythema is difficult to detect in patients with darker pigmented skin.1 It is important that healthcare practitioners understand the differences between lighter [Figure 16-1] and darker [Figure 16-2] pigmented skin.2 Bennett1 defines darker pigmented skin coloration as skin that does not blanch when pressure is applied over a bony prominence [Figure 16-3], irrespective of the patient’s race or ethnicity. Failure to detect signs of inflammation or nonblanching erythema may lead to the development of a life-threatening wound infection.
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The skin is the largest organ in the body whose primary function is to serve as a protective barrier against the environment. Other important functions of the skin include fluid homeostasis, thermoregulation, immune surveillance, sensory detection, and healing. Loss of the integrity the skin due to injury or illness compromises its protective function and, when the loss is extensive, may result in significant disability or even death. It is estimated that in 1996, there were 35.2 million cases of significant skin loss (U.S. figures) that required major therapeutic intervention.3 Of these, approximately 5 million wounds became chronic.
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This chapter covers the basic biology of wound healing, and elucidates different types of wounds, their assessments, treatment and special issues for patients with skin of color.
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WOUND TYPES AND THEIR THERAPY
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Often the etiology of cutaneous wounds stems from a mixture of both intrinsic and extrinsic factors. An example of an intrinsic factor is the genodermatosis, epidermolysis bullosa disorders which predisposes to skin disruption from minor insults such as friction. More mechanistically complex intrinsic conditions, such as venous insufficiency or diabetes mellitus, alter skin architecture and/or its physicochemical properties, leading to ulceration and nonhealing states that are often precipitated by minor trauma. Every ...