Chronic Wounds: Palliative Management for the Frail Population—PART II
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Systemic corticosteroids have direct impact by impairing the physiologic process of wound healing. Nicotine and alcohol use can have profound impacts on wound healing. Many of these patients have lived alone for prolonged periods prior to being placed in a nursing facility. These periods have often been times where medical problems have not been properly addressed, allowing for progressive deterioration of their health, which leads to chronic institutional care.32,33
The first element of a clinical examination is the determination of the history of immobility leading to the inactivity of the calf-muscle pump. This is usually the trigger event that culminates in venous ulceration. A medical history of associated disorders, such as deep vein thrombosis and arterial disease, is important. Previous history of nutritional deficiencies, metabolic disorders, diabetes, collagen vascular disease, antiphospholipid syndrome, periarteritis nodosa, pyoderma gangrenosum, family history of sickle cell disease, thalassemia, hereditary spherocytosis, or any autoimmune disorder should be determined. Time of onset of ulceration may be rapid or slow.
Physical appearance. Venous ulcers are most commonly found on the lower extremities, especially around the malleolus. The wound bed of a venous ulcer exudes copious drainage; a greenish-yellowish, fibrinopurulent, adherent exudate may be seen at the base of the ulcer, which may be highly irregular in shape. Superinfection, pain, and malodorous drainage may ensue. Chronic lower-extremity swelling, often mistaken for originating in cardiac, hepatic, and renal disease, leads to varicosities.
Erythrocytes extravasate into the dermis under pressure and leave behind hemosiderin deposits in the skin or cayenne pepper purpura. A pruritic rash often appears, leading to excoriations and further dermal staining with melanophages as a post-inflammatory event. The topical agents used to keep it under check often aggravate stasis dermatitis. Further acute inflammation produces panniculitis, which becomes more sclerosed with time leading to lipodermatosclerosis. Dystrophic calcium deposits develop sometimes. The exact mechanism by which ulcers result from this long series of events is unknown. It is believed that the capillary fibrin cuff around the vessels and the activity of inflammatory mediators in part derived from white cell entrapment within the cuff all lead to microvascular ischemia. It is possible that minor trauma may also play a role in the ulceration process.
Comorbidities. Venous ulcers are often complicated by comorbidities that include lymphatic obstruction, lymphedema, stasis dermatitis, arthritis, skin rashes, interstitial edema, including bullae microvaricosities, deep vein thromboses, and skin infections (e.g., ecthyma, cellulites). Patients presenting with venous ulcers may have a history of lower-extremity injury, such as a fracture or severe crush injury. Obesity may also accompany the occurrence of venous ulcers, as well as gait abnormalities and arthritis.
Arterial ulcers. Definition. Peripheral arterial occlusive disease (PAOD), which affects the large- and medium-sized vessels, is the most common atherosclerosis disorder of the lower extremities associated with impaired wound healing.34 Patients who develop ulcers or gangrene have impaired circulation to the skin. Arterial stenosis or occlusion impairs blood flow to the extent that despite compensatory mechanisms, the nutritive requirements of peripheral microcirculation cannot be met.35 Ischemia results in tissue necrosis and subsequent ulceration.
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