Chronic Leg Ulcers & Pressure Injuries
Read the wound's site and base, then treat its cause
Approach to the chronic leg ulcer
Sorting the ulcer. Most chronic lower-limb wounds are venous, arterial, neuropathic or pressure-related, and some are mixed. Ask four questions: where is it, what does the base look like, does it hurt, and are pulses present?
Location. Venous ulcers occupy the gaiter area above the medial malleolus. Arterial ulcers are distal: toe tips, lateral malleolus, dorsal foot and sites of minor trauma. Neuropathic ulcers form over plantar pressure points (metatarsal heads, hallux, heel). Pressure injuries overlie bony prominences, most often the sacrum and coccyx, then the heels, the ischial tuberosities of wheelchair users and the greater trochanters.
| Feature | Venous | Arterial | Neuropathic (diabetic) |
|---|---|---|---|
| Ulcer | Shallow, irregular, exudative, red granulation | Punched-out, deep, dry, pale or necrotic base | Deep, punched-out, callus rim |
| Pain | Dull ache, eased by elevation | Severe, worse with elevation and at night | Painless |
| Surrounding skin | Edema, hemosiderin, stasis dermatitis | Cool, shiny, hairless; dependent rubor | Warm, dry, callused |
| Pulses / ABI | Present; ABI usually normal | Absent; ABI ≤0.9 | Often present; ABI may be falsely high |
| First-line care | Compression and elevation once ABI ≥0.8 | Revascularization; no compression | Offloading, debridement, glucose control |
Venous, arterial and neuropathic ulcers
Venous ulcers. The most common leg ulcer (70–80%). Venous hypertension from valve incompetence, prior DVT or calf-pump failure causes capillary leak and pericapillary fibrin cuffing. The ulcer is shallow and irregular with a moist red granulating base and a dull ache relieved by elevation. Look for pitting edema, varicosities, brown hemosiderin staining, itchy stasis dermatitis (emollients plus a topical steroid; avoid sensitizers such as neomycin) and lipodermatosclerosis, a woody fibrosis that tapers the lower calf into an "inverted champagne bottle."
Venous ulcer treatment. Compression (multilayer bandage, Unna boot or 30–40 mmHg stockings) plus elevation above heart level and walking to work the calf pump. Check the ABI first, because compression can necrose an ischemic limb. Adjuncts include pentoxifylline and duplex-guided early ablation of superficial reflux, which speeds healing; lifelong stockings help prevent recurrence.
Arterial ulcers. Round, sharply demarcated, deep, dry ulcers with a pale or necrotic base at distal sites. Pain is severe, worse at night and with elevation, and eased by dangling the leg. The limb is cool with shiny hairless skin, thick nails, absent pulses, elevation pallor and dependent rubor. An ABI ≤0.9 confirms PAD and <0.4 signals severe ischemia; an ABI >1.4 means calcified, noncompressible arteries (diabetes, CKD), so use the toe-brachial index (abnormal <0.7). Healing requires revascularization (endovascular or bypass) plus smoking cessation, a statin and antiplatelet therapy. Never compress, and leave stable dry eschar alone until perfusion is restored.
Neuropathic ulcers. Loss of protective sensation (failed 10-g monofilament) lets repetitive plantar pressure build callus that breaks down into a deep, painless ulcer with a hyperkeratotic rim. The foot is warm with pulses unless PAD coexists, and many ulcers are neuroischemic, so check the ABI anyway. Treat with offloading (a total contact cast is the gold standard), sharp debridement of callus, infection control and glycemic control. Prevent with an annual monofilament exam, daily self-inspection and protective footwear.
Osteomyelitis. A positive probe-to-bone test, an ulcer >2 cm², visible bone or an ESR >70 mm/h makes osteomyelitis likely. X-rays come first but can stay normal for about 2 weeks; MRI is the most sensitive imaging; bone biopsy with culture is the gold standard and guides a prolonged antibiotic course.
Pressure injuries
Mechanism and risk. Pressure over a bony prominence that exceeds capillary perfusion causes ischemic necrosis; shear, friction and moisture add injury. Muscle is more vulnerable than skin, so damage begins at the bone–muscle interface. Risks include immobility (spinal cord injury, stroke, sedation), sensory loss, incontinence, malnutrition and old age. The Braden scale scores six domains (sensory perception, moisture, activity, mobility, nutrition, friction/shear) for a total of 6–23: ≤18 means at risk and ≤9 very high risk.
| Category | Findings | Key distinction |
|---|---|---|
| Stage 1 | Intact skin, nonblanchable erythema | Blanching redness is reactive hyperemia; in dark skin look for warmth, edema, firmness or color change |
| Stage 2 | Partial-thickness loss with pink, moist dermis or a serum-filled blister | No fat, granulation, slough or eschar |
| Stage 3 | Full-thickness loss with visible fat; granulation, epibole, undermining or tunneling possible | No fascia, muscle, tendon, ligament, cartilage or bone |
| Stage 4 | Exposed or palpable fascia, muscle, tendon, ligament, cartilage or bone | Highest osteomyelitis risk |
| Unstageable | Base hidden by slough (yellow/tan) or eschar (brown/black) | Proves to be stage 3 or 4 once debrided |
| Deep tissue injury | Persistent nonblanchable deep red, maroon or purple discoloration, or a blood-filled blister | Deep damage that can rapidly open |
Never reverse-stage: a stage 4 wound that is filling in is charted as a "healing stage 4," not as stage 2.
Prevention.
- Reposition bedbound patients at least every 2 hours with a 30° lateral tilt; seated patients shift weight frequently.
- Use pressure-redistributing surfaces (alternating-pressure, low-air-loss, air-fluidized).
- Keep the head of the bed ≤30° to limit shear, and float the heels off the mattress.
- Control incontinence moisture with barrier products, optimize protein and calories, and inspect skin daily.
Avoid donut-ring cushions and massage of reddened bony prominences; both worsen local ischemia.
Wound care and the atypical ulcer
Moist healing and debridement. Wounds re-epithelialize fastest when moist but not macerated: hydrogel for dry beds, hydrocolloid or film for light exudate, alginate or foam for heavy exudate. Cleanse with saline; wet-to-dry gauze is nonselective and painful. Debride necrotic tissue (sharp is fastest; autolytic, enzymatic, mechanical and larval are alternatives), except stable heel eschar, unrevascularized ischemic ulcers and pyoderma gangrenosum.
Infection. Every chronic wound is colonized, so infection is diagnosed clinically (spreading erythema, warmth, purulence, odor, systemic signs). Culture deep tissue after debridement, or bone if osteomyelitis is suspected. Negative-pressure wound therapy helps deep, clean stage 3–4 wounds, and some stage 4 injuries need flap closure.
When to biopsy. Biopsy the margin of an ulcer that stalls despite weeks of optimal care or looks atypical: rolled or exophytic edge, bleeding, rapid growth or an unusual site. A Marjolin ulcer is an aggressive squamous cell carcinoma arising years to decades later in a chronic wound, burn scar, osteomyelitis sinus tract or long-standing venous ulcer; it metastasizes more often than ordinary cutaneous SCC and needs wide excision.
Pyoderma gangrenosum. A neutrophilic dermatosis: a pustule becomes a rapidly enlarging, very painful ulcer with a violaceous, undermined border, usually on the legs. It accompanies IBD, rheumatoid arthritis and hematologic malignancy or IgA gammopathy. It is a diagnosis of exclusion (biopsy to rule out infection, vasculitis and cancer), and pathergy means debridement or grafting enlarges it. Treat with systemic corticosteroids or cyclosporine, or a TNF inhibitor when IBD coexists; healed lesions leave cribriform scars.
Other mimics. Vasculitis, calciphylaxis (end-stage kidney disease), sickle cell and hydroxyurea-induced ulcers, and atypical infections.