Wound Classification

What are the 4 categories of etiology-based wound classification?

Arterial, venous, pressure, and neuropathic.

What are the causes of acute arterial ischemia?

Trauma, embolism from the heart, or thrombosis at the site of pre-existing chronic arterial occlusion.

What 4 factors determine the extent of tissue necrosis in acute arterial insufficiency?

Site of occlusion, suddenness of occlusion, extent of collateralization, and duration of ischemia.

What are the 5 P's of acute arterial occlusion (a medical emergency)?

Pain, pallor, pulselessness, paresthesia, and paralysis.

What is arteriosclerosis obliterans?

Chronic arterial insufficiency from systemic atherosclerosis: cholesterol deposits narrow the lumen of medium/large arteries, causing fibrosis and calcification.

At what age do arteriosclerosis obliterans symptoms usually start appearing?

Usually after age 50, it progresses slowly over years.

What is intermittent claudication?

Activity-specific ischemic calf muscle pain that stops after ceasing the activity; repeatable and predictable at the same workload.

What is resting claudication?

Pain that occurs even when tissue demands can't be met at rest, indicating complete obstruction.

What does the ankle-brachial index (ABI) measure?

An indirect, noninvasive measure of tissue perfusion, the ratio of systolic BP at the ankle vs the arm.

What ABI value indicates arterial pathology?

Less than 0.90.

What ABI range is the minimum needed for wound healing?

0.40 to 0.50.

What ABI level indicates tissue necrosis?

Less than 0.2 to 0.3.

Where are arterial ulcers typically located?

Dorsum of the foot, toes, and areas of trauma.

What does the wound bed of an arterial ulcer look like?

Regular, "punched out" appearance; pale granulation tissue if any; black eschar; gangrene; minimal drainage.

What periwound skin changes are typical with arterial insufficiency?

Thin, shiny skin; loss of hair growth; pale, dusky, or cyanotic skin.

What pulse findings go with arterial wounds?

Decreased or absent pulses, with an ABI below 0.9.

At what ABI does a non-healing limb wound require revascularization?

0.5 or below; healing won't occur with conservative measures alone.

What are the three lower-extremity bypass surgery locations?

Femoral-popliteal, aorto-femoral (or bifemoral), and femoral-tibial.

What are the main risk factors for arterial ulcers?

Hyperlipidemia, coronary artery disease, smoking, diabetes, hypertension, trauma, and advanced age.

How does nicotine worsen arterial insufficiency?

It vasoconstricts, lowers available oxygen from hemoglobin, increases clot formation and blood viscosity, and enhances cholesterol deposition.

What prevention guidelines help protect against arterial ulcers?

Protect from trauma, self-inspect, minimize caffeine and smoking, control blood pressure/cholesterol/diabetes, take thermal precautions, and moisturize skin.

What regulates venous blood flow toward the heart?

Valves; they direct flow from superficial to deep veins.

What two pumps assist venous return?

The respiratory pump and the calf muscle pump.

What are perforating veins, and where are most of them located?

Veins that pierce the fascia to connect deep and superficial veins; most are located at the "gaiter area."

What causes venous hypertension?

Calf pump failure, incompetent valves, dilation/varicosity, or proximal occlusion/thrombosis; pressure fails to fall after calf muscle contraction.

What percentage of venous ulcers can resolve with conservative treatment?

Up to 90%.

What is the recurrence rate for venous ulcers, and what is it correlated with?

13 to 81%, correlated with nonadherence to treatment.

Where are venous ulcers typically located?

Medial malleolus, medial lower leg, and areas of trauma.

What does the wound bed of a venous ulcer look like?

Irregular, red wound bed with a fibrous yellow or glossy coating and increased drainage.

What periwound signs are seen with venous ulcers?

Edema, cellulitis, and hemosideric (brown) staining.

What is the typical pain pattern for venous ulcers?

Mild to moderate, decreasing with elevation or compression.

What are the main risk factors for venous ulcers?

Vein/valve dysfunction, varicosity, calf muscle pump failure, trauma to an edematous leg, previous ulcer, advanced age, and diabetes.

What size predicts better healing for venous ulcers?

Smaller size, under 10 cm.

What factors predict poor healing of venous ulcers?

Larger size, present over 3 months, growth over the first 4 weeks, deep vein involvement, coexisting arterial insufficiency, older age, high BMI, and poor compliance with compression.

What is the NPIAP definition of a pressure ulcer?

Any lesion caused by unrelieved pressure resulting in damage to underlying tissue.

What are the three mechanical forces that cause pressure injuries?

Pressure (perpendicular force), shear (tangential force), and friction (parallel force).

What is the most common site for pressure ulcers?

The sacrum; 95% occur in the lower half of the body.

What is the number one risk factor for pressure ulcers?

Immobility.

What six categories does the Braden Scale assess?

Sensation, moisture, activity, mobility, nutrition, and friction/shear.

What is the Braden Scale scoring range, and what does a higher score mean?

6 to 24 total; a score of 4 in each category means no problem, so higher scores indicate lower risk.

How long can tissue survive unrelieved pressure before ischemic destruction begins?

About 2 hours, much less in high-risk patients like the elderly or those with diabetes.

What does "tip of the iceberg" mean in pressure injuries?

Necrosis over a bony prominence forms a pyramid shape, base closest to the bone and apex at the skin surface; deep damage often exceeds what's visible on the surface.

What wound shape suggests shear forces caused a pressure injury?

A triangular, teardrop shape.

What must you never do when staging a pressure ulcer?

Reverse stage it.

Describe a Stage I pressure injury.

Non-blanchable erythema on intact skin in light skin tones; in dark skin tones, look for temperature, tissue consistency, or sensation changes instead.

Describe a Stage II pressure injury.

Partial-thickness skin loss of the dermis and/or epidermis, presenting as an abrasion, blister, or shallow crater with a pink-red bed.

Describe a Stage III pressure injury.

Full-thickness skin loss with subcutaneous tissue necrosis, extending to but not through the fascia; presents as a deep crater, possibly with undermining or tunneling.

Describe a Stage IV pressure injury.

Full-thickness loss with damage to muscle, bone, or supporting structures; slough or eschar may be present, and undermining or sinus tracts are common.

What defines a suspected deep tissue injury (DTI)?

Purple or maroon discoloration of intact skin, or a blood-filled blister from underlying soft tissue damage.

When is a pressure ulcer classified as "unstageable"?

When eschar or slough covers the wound base enough that true depth can't be determined.

What percentage of people with diabetes develop a lower-extremity ulcer?

About 15%.

What percentage of diabetic amputations are preceded by a foot ulcer?

About 85%.

What is the classic location of a neuropathic ulcer?

The plantar surface of the foot; the toes are also common.

What monofilament size defines loss of protective sensation?

The 10g (5.07) Semmes-Weinstein monofilament.

What foot deformity results from motor neuropathy in diabetes?

Paralysis of intrinsic foot muscles and shortened plantar fascia, which increase plantar pressure and shear, contributing to Charcot foot.

What autonomic changes contribute to neuropathic ulcers?

Dry, inelastic, cracked skin; increased callus formation; and AV shunting that decreases superficial perfusion while bone resorbs (Charcot foot).

What shape are neuropathic ulcers typically?

Round.

What periwound features are seen with neuropathic ulcers?

Calloused edges, dry skin, and thick toenails.

Why are neuropathic ulcers usually painless?

Because sensory neuropathy blunts protective sensation.

What is Charcot foot?

A midfoot arch collapse that reverses into a rocker-bottom deformity, driven by increased blood flow causing bone resorption.