A chronic wound is defined as an area of skin ulceration of more than six weeks’ duration. In contrast to an acute wound which progresses linearly through the overlapping phases of hemostasis, inflammation, cellular proliferation, and wound remodeling, a chronic, non-healing wound is trapped in a vicious cycle of inflammation, infection, and tissue destruction. In managing non-healing wounds, the following key principles apply:
Establish a diagnosis
Prepare the wound bed
Maintain a moist interactive environment
Administer holistic wound care
A right diagnosis will ensure that the patient receives the right treatment. For instance, the gold standard and most effective way to treat a chronic venous ulcer is by using compression therapy such as the four-layer compression bandaging.
In diabetic foot ulcers, there are often mixed etiologic factors that contribute to poor healing such as macrovascular and microvascular compromise, sensorimotor neuropathy, chronic infection, poor skin barrier function, and repeated injury. Each factor needs to be assessed and managed accordingly, but key priorities include re-establishing an adequate blood supply, off-loading, and protecting critical, pressure areas.
Chronic skin ulcers due to underlying inflammatory or autoimmune disorders often pose a challenging diagnostic and management problem to the dermatologist. As the majority of such ulcers occur on the lower extremities, they may mimic other more commonly encountered conditions, such as venous leg ulcers. Furthermore, new ulcers in an immunosuppressed patient with underlying collagen vascular disease, such as rheumatoid arthritis, may be multi-factorial in etiology. They may result from the disease process itself or from other associated conditions, such as pyoderma gangrenosum, atypical infection, or malignancy.
Important inflammatory ulcers include medium vessel vasculitis, livedoid vasculopathy, and cutaneous polyarteritis nodosa, which may be associated with underlying hepatitis B infection in Asians. Important clinical signs that point toward an underlying vasculitic or inflammatory etiology include palpable purpura, ecchymosis, necrosis, and livedo reticularis. A livedo-like pattern, such as livedo racemosa, may be associated with polyarteritis nodosa, cryoglobulinemia, or hypercoagulable states such as anti-phospholipid syndrome. Inflammatory ulcers, especially those due to livedoid vasculopathy, often heal with atrophie blanche-like scars, which are smooth, stellate-shaped, porcelain-white scars associated with surrounding hyperpigmentation and telangiectasias. Ulcers due to pyoderma gangrenosum often present as rapidly expanding, exquisitely painful lower limb ulcers with a characteristic undermined violaceous border. A full cutaneous and systemic examination should be performed to identify valuable clues such as nail fold infarcts, digital gangrene, calcinosis cutis, peripheral neuropathy, and photosensitivity.
Leprosy as an underlying cause of a neuropathic ulcer must be kept in mind, especially in patients from Asian countries where the disease is still endemic.
Importantly, the vascular status of any ulcer should be assessed clinically by palpating for an arterial pulse or measuring the ankle brachial index as this may have implications on the healing ability of the ulcers.