WCC – Wound Care Certified

Treatment follows etiology. A venous ulcer heals with compression, an arterial ulcer with revascularization, a neuropathic ulcer with offloading, and a pressure injury with pressure redistribution. Choosing the wrong etiology leads to the wrong plan, and in the case of compression on an ischemic limb, to harm. The exam expects candidates to identify wound type from location, appearance, pain pattern, and surrounding skin, and to apply the correct classification system to each.

Depth terminology is used for skin tears, burns, surgical wounds, and vascular ulcers. Pressure injuries are described with the NPIAP staging system rather than partial/full thickness alone, and diabetic foot ulcers use Wagner or University of Texas classifications.

Venous ulcers account for approximately 70% of lower extremity ulcers and result from chronic venous insufficiency with sustained ambulatory venous hypertension. Valve incompetence, venous obstruction, or calf muscle pump failure (from immobility or ankle joint stiffness) prevents the normal drop in venous pressure with walking. Elevated pressure distends capillaries and leaks fibrinogen, red cells, and fluid into tissue. Proposed mechanisms of ulceration include fibrin cuff formation around capillaries, white cell trapping, and growth factor trapping, all contributing to local tissue hypoxia and inflammation.

Venous ulcers typically occur in the gaiter area, especially over the medial malleolus. They are shallow with irregular margins, a ruddy red granular base, and moderate to heavy exudate. Surrounding skin shows hemosiderin staining (brown discoloration from red cell breakdown), lipodermatosclerosis (induration and fibrosis that can create an inverted champagne bottle leg shape), atrophie blanche (ivory-white stellate scars), stasis dermatitis, varicosities, and edema that worsens with dependency. Patients describe aching and heaviness that improve with elevation. Pedal pulses are usually present, though edema may make them hard to palpate.

Management centers on compression therapy after arterial assessment (ABI), leg elevation, calf muscle pump exercise, moisture management of exudate, skin care for dermatitis, and referral for correction of superficial venous reflux when indicated. Sustained graduated compression of about 30–40 mmHg at the ankle is the standard therapeutic level when arterial flow is adequate.

Arterial ulcers result from inadequate perfusion, most often from atherosclerotic peripheral arterial disease (PAD). Risk factors include smoking, diabetes, hypertension, hyperlipidemia, older age, and chronic kidney disease. Ulcers form at the most distal points and over pressure or trauma sites: toes, tips of toes, between toes, dorsum of the foot, lateral malleolus, and heel.

Arterial ulcers are round with a punched-out, well-demarcated appearance, a pale, dry, or necrotic base, and minimal exudate. Surrounding skin is shiny, thin, cool, and hairless, with thickened nails, elevation pallor, and dependent rubor. Capillary refill is delayed and pulses are diminished or absent. Patients report intermittent claudication (cramping with walking relieved by rest) and, in advanced disease, rest pain that is worse at night and relieved by dangling the leg. Arterial ulcers will not heal without adequate perfusion, so vascular referral for possible revascularization is the priority.

Diabetic foot ulcers arise from a triad of peripheral neuropathy, PAD, and impaired immune response, often triggered by repetitive unnoticed trauma. Sensory neuropathy produces loss of protective sensation (LOPS). Motor neuropathy weakens intrinsic foot muscles, causing claw and hammer toes and prominent metatarsal heads. Autonomic neuropathy reduces sweating, producing dry, fissured skin and arteriovenous shunting that can make the foot feel warm despite ischemia. Charcot neuroarthropathy causes joint collapse and deformity such as a rocker-bottom foot; an acute Charcot foot is warm, red, and swollen and must be immobilized and offloaded.

Neuropathic ulcers typically form on the plantar metatarsal heads, great toe, and over bony deformities. They are round with a callused rim, a pink or red base if perfused, and variable depth; pain is often absent. Management includes offloading (total contact casting is the gold standard for plantar forefoot ulcers; removable cast walkers are alternatives), glycemic control, vascular assessment, infection and osteomyelitis evaluation, serial debridement of callus and nonviable tissue, and daily foot inspection with protective footwear.

The Wagner system grades depth and gangrene but does not separately account for ischemia or infection in shallow wounds. The University of Texas (UT) system combines depth grade with a stage for infection and ischemia and better predicts amputation risk.

CEAP classifies chronic venous disease by Clinical signs, Etiology (congenital, primary, secondary), Anatomy (superficial, deep, perforator), and Pathophysiology (reflux, obstruction, or both). The clinical class is most frequently tested.

A pressure injury is localized damage to the skin and underlying soft tissue, usually over a bony prominence or related to a medical or other device, resulting from intense and/or prolonged pressure or pressure in combination with shear. Tissue tolerance is affected by microclimate, nutrition, perfusion, comorbidities, and the condition of the soft tissue. Deep tissue damage often begins at the bone–muscle interface, where pressure is concentrated, and extends outward, which explains why a small skin opening may overlie extensive deeper destruction.

Common sites are the sacrum/coccyx, heels, ischial tuberosities, greater trochanters, occiput, elbows, and scapulae. Seated individuals load the ischial tuberosities; supine individuals load the sacrum and heels; side-lying individuals load the trochanters, lateral malleoli, and ears.

A skin tear is a traumatic wound caused by mechanical forces, including shear, friction, and blunt force, including removal of adhesives. It may be partial thickness (epidermis separates from dermis) or full thickness (both epidermis and dermis separate from underlying structures). Skin tears are most common on the extremities, especially the dorsal hands and forearms and the lower legs, of older adults, neonates, and people on long-term corticosteroids. Contributing factors include dry, fragile skin, prior skin tears, ecchymosis, impaired mobility, dependence for ADLs, cognitive impairment, and polypharmacy.

Management steps: control bleeding, gently cleanse, assess flap viability, and ease the flap back into place (a moistened cotton-tipped applicator or gloved finger can help). Use nonadherent dressings such as silicone contact layers, foam, or hydrogel; avoid adhesive strips, sutures, and staples on fragile skin. Mark an arrow on the dressing indicating the direction of removal — away from the attached flap base — so the flap is not lifted at the next change.

MASD is inflammation and erosion of the epidermis caused by prolonged exposure to moisture and its contents (urine, stool, sweat, wound exudate, mucus, saliva). The four recognized forms are incontinence-associated dermatitis (IAD), intertriginous dermatitis (ITD/intertrigo), periwound MASD, and peristomal MASD. IAD presents as erythema, edema, and erosion with diffuse, poorly defined borders on the perineum, perianal area, buttocks, and inner thighs; satellite papules and pustules suggest secondary candidiasis. Fecal incontinence, particularly liquid stool, is more damaging than urine because of digestive enzymes.

Extent is estimated with the Rule of Nines in adults (head 9%, each arm 9%, anterior trunk 18%, posterior trunk 18%, each leg 18%, perineum 1%) or the Lund-Browder chart, which adjusts for age and is preferred for children. Circumferential full-thickness burns may require escharotomy.

Roughly 10% of chronic wounds are atypical — caused by inflammatory, malignant, infectious, metabolic, or other uncommon processes. Suspect an atypical etiology when a wound is in an unusual location, looks different from typical vascular, pressure, or neuropathic wounds, is disproportionately painful, or fails to improve despite appropriate standard care. A biopsy (often of the wound edge) is indicated when malignancy or an inflammatory process is suspected.