Wounds 101: A Clinician’s Guide to Chronic Wound Assessment, Treatment, and Common Myths

Featured video: Watch the full WHS Education Committee webinar on YouTube

Presenters:

• E. Foy White-Chu, MD, CWSP, AGSF
  • Associate Professor, Oregon Health & Science University; Medical Director, Wound Healing Program, VA Portland Health Care System; Fellow of the American Geriatrics Society
• Lisa J. Gould, MD, PhD, FACS
  • Reconstructive Plastic and Wound Surgeon, South Shore Health, Weymouth, MA; Past President of the Wound Healing Society

 

Wound Types: The Starting Point

Every treatment decision depends on correctly identifying the wound type. The most common chronic wounds fall into a few recognizable categories:

Arterial ulcers are driven by ischemia. They are typically small, deep, painful, and have a punched-out appearance. Perfusion is the clinical question that matters most.

Venous ulcers are caused by venous hypertension. They are usually superficial, can be painful, and appear in the gaiter distribution, the area from the mid-calf to just above the ankle.

Diabetic ulcers are a combination of neuropathy, ischemia, and repetitive pressure. Purely neuropathic ulcers also exist, often from prior trauma or back injury, and these tend to heal better because the diabetic and ischemic components are absent. The pressure problem remains because the patient cannot feel it.

Pressure injuries occur when pressure exceeds capillary perfusion at the tissue interface, leading to hypoxia, ischemia, and necrosis. A reperfusion injury can also occur after offloading if damage has already been done.

Traumatic and surgical wounds round out the common list, with surgical wound complications among the most costly wound types in the healthcare system.

 

Vascular Assessment: What to Check Before Anything Else

Before any treatment plan is built, vascular status must be established. Two urgent findings to rule out at the first visit:

Deep venous thrombosis. Homan’s sign has been shown to be unreliable, lacking both specificity and sensitivity. The real clinical signals are a swollen leg with new calf pain and a color change to red or purple. These patients need an urgent ultrasound.

Limb ischemia. Sudden foot pain, absent pulses, and color change is a limb-threatening emergency.

For perfusion assessment, four elements matter:

• Muscle atrophy, especially in the intrinsic muscles of the foot, where the arch appears hollowed out
• Peripheral pulses, which are notoriously unreliable on palpation alone
• Doppler signals, which range from triphasic (normal) to biphasic, monophasic, or absent. Learning what these sound like is a skill worth developing because fingers alone cannot substitute for a Doppler
• Ankle-Brachial Index (ABI) measurement

Interpreting the ABI

ABI compares ankle pressure to brachial pressure and requires only a blood pressure cuff and a stethoscope. The ranges:

• 0.9 to 1.2 Normal
• Greater than 1.2  Non-compressible vessels, usually from arterial calcification
• 0.6 to 0.9  Mild arterial obstruction
• 0.4 to 0.6  Moderate obstruction
• Less than 0.4  Severe obstruction

Trained clinic nurses can perform ABIs as reliably as non-invasive vascular labs. When lab access is unavailable, the bedside measurement is a strong substitute.

Venous Hypertension and Phlebolymphedema

Venous hypertension is the most common cause of lower extremity wounds, with valve reflux being the primary etiology. Risk factor assessment should include family history, prior lower extremity surgery or trauma (which can disrupt both valves and lymphatics), history of blood clots, and pelvic radiation therapy or cancer, which damage the lymphatic system significantly.

What develops is a two-hit injury. Valve damage leads to reflux. At the same time, the lymphatic system gets overwhelmed and cannot keep up with fluid demands. The result is progressive lower extremity swelling with both venous and lymphatic dysfunction working together, a condition clinicians increasingly refer to as phlebolymphedema.

The Stemmer sign is the bedside test for lymphatic involvement. Pinch the skin over the dorsum of the second toe. In a normal foot, your fingertips will come close to touching. In a patient with lymphedema, the skin is too thick to lift, and your fingertips cannot touch. This is a positive Stemmer sign, and it is diagnostic enough on its own. More advanced lymphatic testing exists, but it is rarely needed clinically.

Why Walking Works (With Compression)

Venous pressure rises significantly when a patient transitions from lying down to standing. In a healthy limb, walking drops those pressures meaningfully. In a limb with superficial or perforator reflux, walking does not reduce venous pressures as effectively. This is important context, but does not mean patients shouldn’t walk. When the limb is compressed, and the patient walks, venous pressures drop and wound healing accelerates.

For further reading on the lymphatic component, see the WHS lymphedema webinar, covering compression bandaging technique, complete decongestive therapy, and long-term management.

Recognizing Venous Leg Ulcers

Classic presentations include:

• Stasis changes with hyperpigmentation and hemosiderin staining
• In darker-skinned patients, stasis changes may appear as simple skin darkening rather than the classic brown pigmentation
• Wounds typically in the gaiter area, though exceptions exist (including venous foot ulcers in patients with spider veins extending into the foot)
• Skin scaling and pruritus from the inflammatory process, which can break down the skin barrier and lead to cellulitis and further wounds

Venous insufficiency is fundamentally an inflammatory disease. White blood cells leak into the interstitial space, driving skin changes and itching. Compression therapy reverses this by clearing the interstitium, which is why compression is so central to venous wound management.

 

Management of Edema-Associated Leg Wounds

The standard of care for venous and mixed venous-lymphatic lower extremity wounds is compression therapy. Internationally, only about 20 percent of patients receive appropriate compression. Closing that gap is the single highest-value intervention most wound programs can make.

Contraindications to compression:

• ABI less than 0.5 or severe peripheral arterial disease
• Acute decompensated heart failure (slow, gentle compression can still be used in coordination with diuresis if the team is aligned)

Compression technique:

• Wrap from the base of the toes to just below the knee
• 50 percent overlap between wraps
• A generous moisturizer to calm the inflammatory process and reduce pruritus
• Use cotton or cast padding rather than rolled gauze. Rolled gauze dries out the skin and sticks, which rips fragile skin on removal
• Tape the top of the cotton padding to the skin to help keep layers from sliding (only appropriate when skin is not fragile)

Exercise prescription:

• Ideal target: 30 minutes of walking, 3 times per week
• Realistic for many patients: 10 minutes, 3 times per day, with physical therapy support if needed
• Add calf raises to activate the calf muscle pump. The combination of compression, walking, and calf raises moves the needle significantly on wound healing

For patients with significant superficial venous insufficiency, vascular surgery consultation for ablation therapy should be considered.

 

Diabetic Foot Ulcers: Recognition and Triage

Diabetic foot ulcers present in several distinct patterns, and the pattern drives urgency.

Neuropathic foot ulcer. The classic presentation is repeated pressure over a bony prominence in an insensate foot. The base appears pale, and callus builds around the edges. 

Charcot foot deformity. Complete collapse of the ankle into the instep creates a rocker-bottom foot. Bone is often exposed, hypergranulation tissue is common, and offloading is difficult while preserving ambulation. Most podiatrists will not reconstruct if the patient remains shoeable.

Plantar tracking infection. Surgical emergency. A small ulcer on the plantar surface of a toe, uncontrolled blood sugars with no clear reason, and the ability to pass a Q-tip from the ulcer along the plantar fascia to the instep. Infection is tracking along the fascia and the patient needs to go to the operating room for emergent incision and drainage.

60-Second Screening for the High-Risk Foot

A validated quick-screen algorithm (Sibbald) identifies the high-risk diabetic foot in under a minute. One or more positive answers warrant referral to a foot specialist or podiatry team:

• Previous ulcer on either foot
• Previous amputation
• Foot deformity
• Ingrown toenails with thickened nail fold
• No pedal pulses
• Active ulcer, blisters, or calluses
• Positive monofilament exam

The monofilament test uses a 10-gram (or, for loss of protective sensation, a 5-gram) filament pressed against the toes and balls of the feet. Test on the leg first so the patient understands the sensation is harmless before you test the foot. Inability to feel the filament indicates loss of protective sensation and a high risk of ulceration.

Pressure Injuries: Prevention and Management

Pressure injuries are a common geriatric syndrome driven by pressure overcoming the capillary interface, producing hypoxia, ischemia, and necrosis. Incontinence does not cause pressure injuries directly, but fecal incontinence in particular lowers the threshold for skin breakdown by disrupting the skin’s acid mantle.

Distinguishing Pressure Injuries from Moisture-Associated Skin Damage

This is one of the most commonly confused diagnoses in wound care, even among highly skilled clinicians. Blinded photo studies have shown that experienced providers struggle to tell the two apart.

Moisture-associated skin damage typically appears in skin folds, often with signs of fungal colonization, and does not progress to full-thickness loss. If a wound has reached subcutaneous tissue, ischemia and necrosis have been involved, and it is not simply moisture damage.

Pressure injuries follow the standard staging system from stage 1 (non-blanching erythema) through stage 4 (full-thickness with exposed bone, tendon, or muscle), plus unstageable and deep tissue injury categories.

The Hidden Driver: Friction and Shear

Patients in hospital beds with the head of the bed above 30 degrees constantly slide down. Staff then reposition them back up, creating repeated shear forces. Shear reduces the amount of pressure needed to cause hypoxia and necrosis.

Practical steps:

• Keep the head of the bed under 30 degrees when clinically possible
• Use friction-reducing devices under the patient for transfers and repositioning
• Turn every 2 to 4 hours (studies have shown no significant difference in pressure injury rates between 2, 3, and 4 hour intervals, but not beyond 4 hours)

Wheelchair Assessment Is Not Optional

Every wheelchair user should have a formal wheelchair assessment, and not just a cushion evaluation. Ask patients where their chair came from. If it’s from a big-box store rather than a seating specialist (typically a PT or OT), the chair is likely not a good fit for them.

Wheelchairs should be reassessed annually and whenever the patient has a major weight change. Significant weight gain creates pressure from side rails and lateral thigh contact. Significant weight loss produces a frail, slumping patient who is no longer positioned correctly.

Additional Prevention Strategies

• Group 1 high-viscosity foam mattresses for high-risk patients (covered by Medicare with appropriate documentation)
• Dimethicone-based barrier creams for fecal incontinence
• Prophylactic silicone-bordered foam over bony prominences in the ICU setting (strong trial evidence)

When to Call a Surgeon

Not every wound needs a surgeon, but some absolutely do. The clearest indications:

• Large hematomas in anticoagulated patients, especially after a fall or bump
• Warfarin necrosis, typically shortly after warfarin initiation, extremely painful
• Necrotizing soft tissue infection, which does not require a CT scan to diagnose if clinical signs are present
• Plantar tracking diabetic foot infections
• Exposed hardware, which will require a flap for coverage
• Any wound where pain cannot be managed at the bedside

The broader principle: wound care is a team sport. Effective programs integrate podiatry, nurse practitioners, hospitalists, and wound-focused physicians, with surgical consultation when flaps, grafts, or operative debridement are needed.

Wound Assessment: The MEASURE-B Framework

MEASURE-B is a structured approach to wound documentation and reassessment:

• Measure (length, width, depth)
• Exudate (amount, type, color, odor)
• Appearance
• Suffering (pain)
• Undermining and tunneling
• Re-evaluate
• Edge
• Bioburden

Measurement

Mobile apps now do a reasonable job of wound measurement. For manual technique, measure the longest length by the widest width at 90 degrees, or use the clock method. The critical requirement is consistency. If the patient must be rolled to one side, document the position (e.g., “left lateral decubitus”) and measure in the same position each time.

Exudate

Exudate assessment should capture:

• Amount relative to dressing change interval. A dressing that was changed that morning and is already saturated signals uncontrolled drainage
• Color and quality. Serosanguinous (yellow-pink) is the target. Frank blood suggests ongoing bleeding, retraumatization, or anticoagulation effects. Thick white pus suggests infection
• Odor. Many wound products produce odor. Rotten-flesh odor is not normal

The dressing choice and change frequency follow from exudate volume and character. The goal is a dressing that can be left in place as long as possible while still controlling drainage.

Undermining and Tunneling

Gently probing a wound with a Q-tip, gloved finger or, when a tunnel is very narrow a metal probe, does not introduce bacteria. Bacteria are already there. What probing does is reveal the actual wound dimensions and identify any bony contact, which changes clinical management significantly.

Edge Assessment

The edge is where keratinocytes migrate from, so edge quality drives healing progress. Key patterns to recognize:

• Hyperkeratotic edge. A small granular wound may be surrounded by thick hyperkeratotic skin that is actually the true wound boundary. Sharp debridement parallel to the skin edge reveals the real wound size
• Rolled edge (epibole). Keratinocytes have grown too quickly and rolled under. They will not migrate across the wound until the rolled edge is shaved flush with the wound bed
• Callus. Similar to hyperkeratosis, but the callus itself produces additional pressure that drives ischemia underneath. Debride it to the actual skin edge
• Maceration. Ask whether it is from wound drainage (change the dressing) or external sources like bathing, weather, or incontinence
• Erythema. Bright red erythema extending 2 cm or more from the wound edge raises concern for significant infection
• Baby epithelium. Pink or lavender, very fragile, migrating inward. This is the goal

Wound Bed Appearance

Healthy granulation tissue is deep pink or red, firm, and granular, with healthy migrating epithelium at the edge. Sometimes new epithelium can look purple, which is normal and should be monitored rather than disturbed.

Non-viable tissue to debride:

• Black or brown eschar (assuming adequate arterial flow)
• Yellow fibrinous tissue, either firm or slimy
• Hypergranulation tissue, which can indicate inflammation or high bioburden

Moist Wound Healing: The Foundation

Modern wound care is built on Winter’s 1960s experiments with pig dermis, which showed that wounds covered with a polyethylene film healed faster than those left exposed to air. Exposed wounds formed fibrinous tissue that blocked epithelial migration. Covered wounds allowed leukocytes to exit with exudate, leaving the epithelium free to migrate.

The clinical principle: a dry wound forms eschar that blocks epithelial migration. A wet wound damages surrounding tissue, macerates the edge, and invites biofilm. The target is moisture balance.

There is a place for eschar. It blocks bacterial entry and is acceptable in some clinical contexts. The trade-off is prolonged healing time, and as long as the wound remains open, infection risk is elevated.

Dressing Categories and What They Do

Dressings that add or retain moisture:

• Hydrogels
• Hydrocolloids
• Vaseline or oil-based products

Dressings that remove moisture:

• Alginates
• Hydrofibers
• Foams
• Extra-absorbent composite dressings

Most wound care uses a primary dressing (in contact with the wound) and a secondary dressing (wicking fluid away from the periwound). Engineering has produced many sophisticated options. The best dressing is the one that the patient can actually get, that controls exudate between changes, that does not cause pain, and that does not need changing too often.

 

Debridement: The Tools and the Reasoning

Debridement removes non-viable tissue, bioburden, and debris so the wound can progress. Options include:

Sharp debridement with scalpel, dermal curette, or scissors. This is the most rapid method if within the clinician’s scope of practice and the patient’s tolerance and goals of care.

Ultrasonic debridement. Effective and can be performed by trained nurses.

Autolytic debridement. Uses the patient’s own proteases, aided by hydrogels, hydrocolloids, or films that keep the wound moist. It’s slow but painless, and often used for infants with eschar from IV extravasation because a clear film allows monitoring without pain.

Enzymatic debridement. Faster than autolytic but still slow. Requires daily dressing changes as a drug delivery, though three-times-weekly has worked for some older adult patients with visiting nurse support.

Biologic debridement (medical maggots). Highly selective, only eating dead tissue. Useful as a palliative care option. They come in tea bags rather than free-range.

How Often to Debride

A study of 312,000 wounds across 525 wound centers showed that patients debrided weekly early in treatment healed more wounds in shorter timeframes. The mechanism: reduced bacterial burden, reduced inflammation, and reduced senescent cells.

But more is not always better. The need for debridement should decline over time as the wound progresses. Billing incentives have pushed some programs toward over-debridement. The appropriate curve starts with weekly debridement early, the frequency and intensity then tapers as dressings provide appropriate management.

 

Infection Diagnosis: Contamination, Colonization, and Clinical Infection

All open wounds are contaminated. Staph and strep live on skin and will be in the wound. This is why routine wound cultures are not useful. The distinction between contamination and infection is what drives clinical action.

The Infection Continuum

The International Wound Infection Institute framework describes:

• Contamination. Bacteria present, no clinical impact
• Colonization. Bacteria multiplying, no clinical impact
• Covert infection. Hypergranulation, tissue that bleeds easily with contact, pocketing under the epithelium, increased drainage, stalled healing
• Overt infection. Erythema, warmth, swelling, possible purulence, wound breakdown
• Spreading infection. Erythema extending more than 2 cm from the wound edge requires systemic antibiotics
• Systemic infection. Sepsis requires hospitalization. Patients can die from wound infections

Lab Testing Limitations

Standard lab markers are inexact:

• CRP and ESR can be elevated from many causes, not just wound infection
• White blood cell count is non-specific. Many wound consultations turn out to be urinary tract infections
• Procalcitonin elevates with severe infection but does not track cellulitis, and does not guide antibiotic decisions
• IL-6 would be specific for early wound infection, but is not clinically available

Cellulitis Is Frequently Overdiagnosed

Many patients hospitalized with presumed cellulitis improve primarily because their legs are elevated and edema decreases, not because of antibiotics. The underlying diagnosis is often stasis dermatitis that clears with elevation.

When evaluating apparent cellulitis, consider:

• Is this stasis dermatitis rather than infection?
• Is there poorly controlled drainage irritating the periwound?
• Is there a critical bacterial count requiring topical antimicrobials?
• Is there trauma or pressure to the area?
• Is this moisture-associated skin damage?

If cellulitis is not improving with treatment, the underlying driver is probably not infection.

When a Culture Is Warranted

Biopsy and aspiration remain the gold standard. Validated swab techniques include:

• Levine technique. Press to express wound fluid, then rotate the swab 360 degrees in a 1 cm² area of the cleanest wound bed
• Essen Rotary technique. Press and rotate from the wound center outward. Equal or possibly superior validation compared to Levine

Even with culture, results are qualitative, not quantitative.

For biopsies, check your lab’s specific requirements. Typical specifications include a 3 mm cube specimen on 2×2 gauze in a sterile container. Punch biopsy or curetted specimens both work. Send fresh and fast.

 

Wound Cleansing

Every wound should be cleansed at every dressing change. Any vendor claiming their product eliminates the need for cleansing should be politely declined.

No solution has proven superior in head-to-head trials. Saline or tap water is acceptable for routine cleansing. Antiseptics become necessary in specific circumstances:

• Critically ill patients
• High bacterial burden
• Significant odor

Options include:

• Dilute Povidone-iodine. Acceptable
• Sodium hypochlorite. Pay attention to concentration
• Acetic acid. Useful for suspected pseudomonas (fluorescent green drainage)
• Hypochlorous acid. Broad spectrum, reportedly antifungal, reportedly less cytotoxic. 

None of these have been validated in rigorous head-to-head trials.

 

Topical Antimicrobials

When bioburden needs direct management:

• Silver (Ag) is bactericidal. Look for “Ag” in dressing names
• Cadexomer iodine slowly absorbs exudate and releases iodine over time, theoretically reducing cytotoxicity
• Medical-grade honey has both bactericidal and bacteriostatic properties
• Gentian violet is bacteriostatic

Avoid topical antibiotics. Anything that would be given systemically should not be applied topically. The risk of driving resistance outweighs the benefit.

 

Protecting the Periwound

Two common tools:

• Skin preps (transparent films) applied to the periwound and allowed to dry. Tape adheres to the film rather than the skin, preventing skin tears on removal
• Zinc-based barriers applied to the wound edge to dry maceration and protect skin

 

Building Your Wound Care Toolkit

For clinicians outside formal wound centers, the essential toolkit is smaller than most assume:

• Documentation: Doppler, eyes, ruler, camera
• Cleansing: Saline or tap water
• Cover: Wet it if dry, dry it if wet. Pick any reasonable dressing category
• Secure: Skin-friendly tape, rolled gauze, or compression wrap

That is the complete toolkit. With these elements and a sound assessment, most clinicians can make meaningful progress on most chronic wounds.

 

Common Myths, Debunked

Myth: Alcohol and hydrogen peroxide are good wound cleansers. Both are cytotoxic to every cell from the edge through the wound bed. Use soap and water for leg wounds, especially during dressing changes, then pat dry and moisturize the periwound.

Myth: Triple-antibiotic ointment (Neosporin and similar) is a good topical. Risk of bacterial resistance and high rates of contact allergy, which is already elevated in patients with chronic wounds. 

Myth: Iodine is always harmful. Iodine has a place, particularly in life-limiting illnesses or critically ill patients where sepsis prevention is the priority.

Myth: What you put on the wound is the most important decision. The dressing does not matter if the foundational issues are not addressed. Foundational factors include:

• Pressure offloading
• Edema management
• Nutrition
• Glucose control
• Adequate blood flow
• Absence of infection

Writing a Wound Care Order

Home health nurses and clinic nurses are seeing many patients. A wound care order that is dense, confusing, or contradictory will not be executed well. Principles:

• Use bullet points
• Keep instructions succinct
• Avoid multiple different treatments on multiple areas when possible
• When different wounds need different care, specify locations clearly
• Follow the sequence: cleanse with, protect, apply, cover, secure

Exceptions to the Rules

Every rule has exceptions. A few worth flagging:

Stable heel eschar. Offload, keep clean and dry. Do not place an occlusive dressing on it. Only consider debridement if arterial flow is adequate and the patient’s goal is to walk.

Ventilated patients with sacral pressure injuries. A patient in a hypercatabolic state will not heal the wound while the body is fighting for brain, heart, lungs, and kidneys. Shift the priority to infection prevention and wound stability until the patient is off the ventilator. Then shift back to healing.

Fecal incontinence with sacral pressure injury. If negative pressure wound therapy cannot contain the wound, consider antiseptic soaked gauze changed with each incontinent episode. Only feasible at home with a dedicated caregiver.

Key Takeaways for Wound Care Clinicians

1. Identify the wound type before anything else. Treatment plans diverge sharply by type.
2. Establish vascular status. Compression without perfusion assessment can cause harm.
3. The Stemmer sign is the bedside test for lymphatic involvement. Learn it.
4. Most venous leg ulcers heal with proper compression, walking, and time. The gap is adoption, not knowledge.
5. Pressure injuries are prevented by assessing the wheelchair, managing friction and shear, and turning every 2 to 4 hours.
6. MEASURE-B is a structured framework for reassessment. Use it consistently.
7. All open wounds are contaminated. Treat only clinical infection.
8. Most wound cultures are unnecessary. When indicated, use validated technique.
9. The foundational issues matter more than the dressing choice.
10. Wound care is a team sport. Know when to call a surgeon.

Watch the Full Webinar

The full recording, including slide content, clinical photos, and Q&A, is available on the WHS YouTube channel and in member-only accounts on the WHS website.

Continue Learning

• Managing Lower Extremity Lymphedema in the Wound Care Setting 
  • Companion article covering compression bandaging, CDT, and lymphedema management in depth
• Chronic Pelvic Pressure Wounds and Osteomyelitis 
  • Dr. Gould’s follow-up session with Christina Megal
• Palliative Care Ulcers 
  • Dr. White-Chu’s previous webinar on wound care in life-limiting illness

This article is a summary of a WHS Education Committee webinar presented on February 18, 2026, featuring Dr. E. Foy White-Chu and Dr. Lisa J. Gould. It is intended as a clinical reference for wound care professionals and does not replace formal medical training or clinical judgment. The WHS Education Committee does not endorse specific commercial products.