5.2 Arterial / LEAD Ulcer Assessment and PAD Testing

5.2 Arterial / LEAD Ulcer Assessment and PAD Testing

Quick Answer: Lower-extremity arterial disease (LEAD) ulcers appear on distal toes, the lateral malleolus, and other pressure points. They look punched-out, with a pale or necrotic base and little drainage. The foot may show hair loss, elevational pallor, and dependent rubor. Pulses are often weak. Apply ABI, TBI, and waveforms here as etiology tests. Do not debride stable dry ischemic eschar on a poorly perfused heel. Tissue loss plus ischemia is chronic limb-threatening ischemia and needs urgent vascular referral.

If section 5.1 was the wet, stained gaiter, this section is the pale, painful, distal wound. Independent OpenExamPrep teaching applies the perfusion numbers you already met in the diagnostics chapter to why this ulcer exists and what you must not do to it.

Location and morphology of LEAD ulcers

Arterial ulcers follow end-arterial territory and trauma. Common sites:

• Distal toes and interdigital spaces
• Lateral malleolus
• Anterior tibial surface
• Heels and other pressure points in a person who cannot reposition, especially when the same heel also lacks inflow

Punched-out means a steep, even edge as if a hole punch removed a circle of skin. The base is pale, gray, yellow, or frankly necrotic. Granulation, if present, is often dull rather than ruddy. Exudate is minimal unless infection or mixed venous disease supervenes; a dripping arterial ulcer should make you look for another process (infection, edema, lymphatic leak) rather than assume “arterial wounds are always wet.”

Surrounding skin may be shiny, taut, and hairless. Nails can be thick and dystrophic. The foot is often cooler than the other side. A narrow “bloodless” margin around the ulcer is a perfusion clue, not poor cleansing.

Contrast this with LEVD: arterial ulcers are usually smaller, deeper-appearing relative to their area, drier, and more distal. A large, irregular, heavily draining medial gaiter wound is a poor arterial prototype even if the patient has a smoking history.

Symptoms you must ask for: claudication, rest pain, hanging-leg nights

Claudication is reproducible muscle pain (calf, thigh, or buttock) after a predictable walking distance that eases with standing still. Not every person with PAD can walk far enough to report it—frailty, neuropathy, and arthritis mute the story.

Rest pain is ischemic pain at rest, typically in the forefoot or toes, worse when the patient is supine in bed. Classic behavior is dangling the leg over the side of the bed or sleeping in a chair so gravity increases a trickle of flow. Document nocturnal hanging-leg behavior; it is high-yield and easy to miss if you only ask “do your legs hurt.” Elevation that worsens pain argues against a purely venous ache.

Ask about tobacco, diabetes, chronic kidney disease, known coronary or carotid disease, and prior bypass or stents. Those facts do not diagnose the wound by themselves, but they raise the prior probability that a lateral ankle hole is arterial.

Bedside perfusion exam: apply ABI, TBI, and waveforms to etiology

Palpate dorsalis pedis and posterior tibial pulses on both feet and grade them. Bounding calcified vessels can still feed a dying toe; absent pulses need Doppler before you write “no flow.” Capillary refill longer than about 3 seconds supports ischemia when the room is warm enough to interpret it.

Elevational pallor: raise the leg about 45–60 degrees for 30–60 seconds. Marked paleness of the sole or toes is an arterial sign. Dependent rubor: a delayed brick-red flush when the leg hangs, which blanches again when the limb is lifted, is ischemic—not cellulitis. Cellulitis stays warm and tender and does not vanish in seconds with elevation.

Now use the numbers you already know as etiology tools:

Waveforms matter when the ratio is confusing. A monophasic ankle signal plus a necrotic toe is LEAD even if someone once documented a “normal” pulse. TBI belongs in diabetes and CKD when ankle vessels are stiff. You are not repeating the entire vascular-lab chapter; you are answering is this ulcer ischemic, mixed, or safe to compress?

Inspect footwear, socks, and both feet—including the heel that the patient cannot see. A new “blister” on a lateral toe after tight shoes in PAD is an arterial ulcer in the making, not a minor nursing note.

Stable dry ischemic eschar: do not “clean it off”

A stable, dry, adherent, non-fluctuant black eschar on a heel with poor pulses, a low ABI or low TBI, and no drainage is a biologic dressing. Do not sharp-debride that scab on a poorly perfused limb in order to “see the wound bed.” Opening ischemic tissue invites wet necrosis and infection you cannot deliver blood to fight. Protect the heel from pressure, keep the eschar dry, watch daily for drainage, odor, bogginess, erythema, or fluctuation, and involve vascular medicine. If the eschar becomes wet, boggy, or there is advancing cellulitis or gas, the plan changes—that is no longer a stable eschar.

This rule is etiology-specific. Moist slough in a well-perfused venous ulcer is a different debridement conversation. The exam loves the poorly perfused heel because the wrong reflex is to pick at black tissue.

CLTI and the threatened limb

Chronic limb-threatening ischemia (CLTI) is PAD with rest pain, gangrene, or ulceration attributable to poor perfusion—tissue loss plus ischemia, not a purely neuropathic plantar ulcer with bounding pulses. Older teaching said “critical limb ischemia”; CLTI is the current threatened-limb frame. A CWCN does not stent the SFA, but a CWCN does stop local tinkering and refer urgently when an ischemic wound appears, when rest pain is present, or when ABI/TBI shows severe disease with tissue loss. Delay for “one more week of hydrogel” is how toes are lost.

Gangrene of a toe, rest pain that prevents sleep, and a new heel ulcer with an ABI of 0.38 are the same family of emergency: vascular, not dressing, first. Infection plus ischemia is even more time-sensitive (wet gangrene).

Scenario: the hanging-leg heel

A 78-year-old man with a 40-pack-year history sleeps in a recliner because his right toes burn when he lies flat. There is a 1.2 cm punched-out ulcer on the lateral right fifth toe, a pale base, scant drainage, and no hair on the toes. The right foot turns brick-red after two minutes of dependency and blanches when you raise it. PT pulse is absent; Doppler is monophasic. ABI is 0.41. A covering nurse asks whether to “unroof the dry black patch on the right heel so we can stage it.” The CWCN documents LEAD ulceration with rest pain and threatened-limb perfusion, holds compression, leaves the dry heel eschar intact, offloads the heel, and arranges same-day or next-day vascular referral rather than a sharp debridement visit. Staging a pressure injury can wait; converting a sealed ischemic heel into an open wound cannot be undone.

Arterial assessment is a stop rule: if location, color change with elevation, pulses, and ABI/TBI say ischemia, the etiology is LEAD until revascularization options are addressed—even if a pressure component also exists on that heel.