WCC cheat sheet

Skin layers: epidermis (avascular, keratinized barrier), dermis (collagen, elastin, vessels, nerves, appendages), and hypodermis (adipose and fascia).

Epidermal oxygen and nutrients arrive by diffusion from the dermis; the stratum basale supplies keratinocytes for re-epithelialization.

The dermis is predominantly type I collagen; fibroblasts synthesize collagen, and myofibroblasts mediate wound contraction.

Hemostasis: immediate vasoconstriction, platelet plug formation, and fibrin clot, providing a provisional matrix.

Inflammation: days 0-4; neutrophils then macrophages remove bacteria and debris; chronic wounds often remain stalled in this phase.

Proliferation: about day 3 to 3 weeks; granulation tissue, angiogenesis, epithelialization, and wound contraction.

Maturation/remodeling: weeks to years; type III collagen is replaced by type I; tensile strength reaches about 80% of uninjured skin.

Moist wound healing increases epithelialization rate compared with dry healing and is a basis for occlusive dressing selection.

Skin surface pH is mildly acidic (about 4.7-5.75), supporting barrier function and antimicrobial defense.

Measure length head-to-toe and width perpendicular to length, both in centimeters; report area as cm² for simple wounds.

Clock face for undermining/tunneling: patient's head is 12 o'clock and feet are 6 o'clock; record direction and depth in cm.

Document location, etiology/stage, size, depth, wound bed tissue percentages, exudate, periwound skin, edges, odor, pain, and infection signs.

Exudate amount descriptors: none, minimal, moderate, large; type: serous, sanguineous, serosanguineous, or purulent.

PUSH tool totals area, exudate amount, and tissue type; score range 0-17; higher score indicates worse wound status.

Braden Scale has six subscales; total 6-23; lower scores indicate higher pressure injury risk; ≤18 commonly triggers prevention.

Trace irregular wound perimeter or use digital planimetry; serial photographs need consent, consistent lighting, and a scale marker.

Wound depth is the deepest point; pressure injury staging is not determined by depth alone once eschar obscures the base.

Reassess and document at least weekly for chronic wounds and more often with infection or deterioration.

Pressure injury: localized damage to skin and/or underlying tissue over a bony prominence from pressure and/or shear.

Stage 1: intact skin with non-blanchable erythema; darker skin may show persistent color change without blanching.

Stage 2: partial-thickness loss with exposed dermis; viable pink/red wound bed; no slough, eschar, or bruising.

Stage 3: full-thickness loss; adipose visible; fascia, muscle, tendon, cartilage, and bone are not exposed.

Stage 4: full-thickness loss with exposed fascia, muscle, tendon, cartilage, or bone.

Unstageable: base obscured by slough/eschar; deep tissue pressure injury: persistent deep maroon/purple discoloration or blood-filled blister.

Do not reverse-stage a healing pressure injury; document current stage and healed status separately.

Reposition at least every 2 hours in bed and every 15 minutes in a chair when able; use 30-degree lateral tilt.

Offload heels with pillows or suspension devices; common sites are sacrum/coccyx, ischium, trochanter, and heel.

Venous ulcer: medial malleolus/gaiter area, shallow, irregular, moist, edema, hemosiderin staining, lipodermatosclerosis; pulses often present.

Compression is the cornerstone for venous ulcers when arterial perfusion is adequate; typical ankle pressure is 30-40 mmHg.

ABI = ankle systolic pressure ÷ brachial systolic pressure.

ABI <0.8 suggests arterial disease; <0.5 severe ischemia; >1.3 suggests noncompressible calcified arteries.

Arterial ulcer: distal/lateral, punched-out, dry, pale, painful, cold, hairless, shiny skin, weak pulses; avoid compression with critical ischemia.

Do not apply high compression when ABI <0.6-0.8 or critical limb ischemia is present; refer for vascular assessment.

Lymphatic/lymphovenous ulcer: edema, hyperkeratosis, papillomatosis, lymphorrhea; treat with decongestive therapy and compression if arterial flow permits.

Elevate legs above heart level for venous edema when no arterial compromise; avoid prolonged dependency.

Mixed arterial-venous ulcers: assess and treat arterial insufficiency first; use modified compression only under supervision.

Neuropathy causes loss of protective sensation; screen with 10-g monofilament plus vibration/temperature and inspect for callus and deformity.

Diabetic plantar ulcers commonly occur at metatarsal heads, hallux, and heel from pressure, shear, neuropathy, and ischemia.

Offload plantar neuropathic ulcers with total contact cast or irremovable walker; removable devices are less effective.

Assess perfusion before debridement; ischemic ulcers need revascularization evaluation, not routine sharp debridement.

Positive probe-to-bone test raises osteomyelitis suspicion; obtain imaging and specialist referral.

Infection signs include erythema, warmth, induration, and purulence; deep or systemic infection is limb-threatening.

Charcot arthropathy: warm, red, swollen foot; offload immediately and refer to prevent deformity.

Daily foot inspection and protective footwear with adequate toe box; avoid barefoot walking.

TIME: T issue nonviable, Infection/inflammation, Moisture imbalance, Edge nonadvancing.

Debridement methods: sharp/surgical, mechanical, enzymatic, autolytic, and biologic/larval.

Autolytic debridement is selective and slow; it uses moisture-retentive dressings and requires adequate perfusion.

Enzymatic debridement uses collagenase; it requires a moist wound environment and appropriate exudate control.

Sharp debridement is contraindicated in unassessed arterial insufficiency, coagulopathy, or ischemic tissue.

Mechanical wet-to-dry debridement is nonselective and painful; avoid for clean granulating wounds.

Stable dry eschar on an ischemic heel should not be debrided until vascular status is evaluated.

Biofilm and rolled/epibole edges may require debridement to restore a healing wound bed.

Bioburden continuum: contamination → colonization → critical colonization → infection.

Infection signs: erythema, warmth, swelling, pain, purulence, odor, delayed healing; systemic signs include fever and leukocytosis.

Biofilm is polymicrobial, adherent, antibiotic-tolerant, and requires mechanical disruption plus antimicrobial therapy.

Culture chronic wounds only with clinical infection; obtain tissue biopsy or deep swab after cleansing, not a superficial swab.

Topical antiseptics include silver, iodine, PHMB, and hypochlorous acid; use for limited periods and reassess.

Systemic antibiotics treat cellulitis, deep infection, osteomyelitis, and systemic signs; they are not for colonization.

Stewardship: culture-directed, narrowest effective agent, shortest duration, and avoid routine topical antibiotics such as neomycin.

High bioburden warrants cleansing and debridement at dressing changes plus appropriate topical antimicrobial.

Select dressings by exudate amount, tissue type, infection status, pain, periwound skin, and goal (debridement, protection, absorption).

Hydrocolloid: low-moderate exudate, intact or partial-thickness wounds; occlusive; avoid on infected wounds.

Hydrogel: dry or minimally exudating wounds; rehydrates and supports autolysis; can macerate surrounding skin.

Foam: moderate-high exudate; absorbent; compatible with compression bandaging.

Alginate/hydrofiber: high exudate; gels in the wound; requires secondary dressing; avoid on dry wounds.

Transparent film: protection of superficial wounds with no exudate; not for infected or draining wounds.

Silver dressings: infected or critically colonized wounds; avoid prolonged routine use.

Negative pressure wound therapy: deep/acute wounds; contraindicated with malignancy, untreated osteomyelitis, or exposed vessels/nerves.

Zinc oxide or barrier films protect periwound skin from maceration and adhesive injury.

Use validated nutrition screens (MUST, MNA); albumin and prealbumin are not reliable markers of wound healing status.

Pressure injury with malnutrition: about 30-35 kcal/kg/day and 1.25-1.5 g protein/kg/day.

Hydration about 30 mL/kg/day unless fluid-restricted; dehydration impairs perfusion and healing.

Vitamin C and zinc support collagen synthesis; supplement when deficient rather than routinely high-dose.

Assess pain with a validated scale; premedicate before dressing changes based on analgesic onset.

Use nonadherent dressings and gentle cleansing to reduce dressing-change pain and skin trauma.

Teach-back confirms caregiver understanding of offloading, repositioning, skin checks, nutrition, and warning signs.

Smoking cessation and glycemic control improve tissue perfusion and wound healing.