Chart — Wound Care
Skin Integrity Risk Factors Chart
Seven major skin integrity risk factors — immobility, malnutrition, moisture, friction, shear, diabetes, and poor perfusion: mechanism of skin injury, assessment focus, and prevention strategies.
Data Source: NPIAP / Braden Scale / WOCN Clinical Guidelines
Educational use only. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
Risk Factor Overview
| Risk Factor | Mechanism (brief) | Key Assessment Tool | Priority Prevention |
|---|---|---|---|
| Immobility | Sustained pressure → capillary closure → ischemia | Braden: Activity + Mobility | Reposition q2h; pressure redistribution surface; float heels |
| Malnutrition | Impairs collagen synthesis and immune response | Braden: Nutrition; Dietitian consult | Protein 1.25–1.5 g/kg/day; Vit C; Zinc |
| Moisture | Maceration → epidermal barrier breakdown; IAD | Braden: Moisture; incontinence assessment | Moisture barriers; timed incontinence care; fecal management |
| Friction | Skin dragged across surface → epidermal abrasion | Braden: Friction & Shear; heel/elbow skin | Lift, don't drag; protective film dressings; heel protectors |
| Shear | Deep tissue tears from skeleton sliding under skin | Braden: Friction & Shear; HOB elevation | Limit HOB >30°; knee-break positioning; low-shear surfaces |
| Diabetes | Neuropathy + vasculopathy + immune dysfunction | Monofilament test; ABI; daily foot check | Glycemic control; therapeutic footwear; daily foot inspection |
| Poor Perfusion | Inadequate O2 delivery → ischemic injury threshold lowered | Peripheral pulses; ABI; hemoglobin | Optimize hemodynamics; anemia treatment; smoking cessation |
Detailed Risk Factor Cards
Immobility
Braden: Activity + MobilityMechanism: Prolonged pressure on bony prominences → capillary closure → tissue ischemia → cell death. Interface pressure >32 mmHg (capillary closing pressure) for sustained periods causes irreversible tissue damage.
Assessment Focus
- Ability to reposition independently (bed mobility, transfers)
- Frequency of spontaneous movement
- Braden Scale: Activity and Mobility subscales
- Sedation and paralytic medications
- Contractures limiting positioning
Prevention Strategies
- Reposition every 2 hours in bed; every 15–30 minutes in chair
- Pressure redistribution support surface (pressure-relieving mattress/cushion)
- 30-degree lateral positioning instead of 90-degree tilt to bony prominences
- Heel elevation off bed surface (pillow under calves) — heels are highest risk sites
- ROM and mobility programs to restore movement capacity
Malnutrition
Braden: NutritionMechanism: Protein deficiency impairs collagen synthesis and immune response. Vitamin C deficiency prevents collagen cross-linking. Zinc deficiency impairs epithelialization. Inadequate caloric intake causes catabolism of structural tissue. Malnutrition is both a cause and consequence of pressure injury.
Assessment Focus
- Weight loss history (> 5% in 30 days or > 10% in 6 months is significant)
- BMI, albumin, prealbumin (limited utility acutely), nitrogen balance
- Appetite and oral intake
- Braden Scale: Nutrition subscale (excellent/adequate/probably inadequate/very poor)
- Malnutrition Screening Tool (MST) or MUST score
Prevention Strategies
- Nutritional assessment by dietitian for high-risk patients
- Ensure protein intake 1.25–1.5 g/kg/day for wound healing
- Vitamin C and zinc supplementation for deficient patients
- Oral supplements if PO intake inadequate
- Enteral or parenteral nutrition if oral route insufficient
Moisture
Braden: MoistureMechanism: Prolonged exposure to moisture (urine, stool, wound drainage, diaphoresis) softens (macerates) skin, breaks down the epidermal barrier, increases friction coefficient, and allows bacteria to penetrate. Incontinence-associated dermatitis (IAD) is distinct from pressure injury but coexist and compound each other.
Assessment Focus
- Incontinence — urinary and/or fecal (frequency, consistency)
- Diaphoresis (fever, sepsis, heart failure)
- Wound drainage quantity and containment
- Presence of IAD: perianal/perineal erythema, skin erosion from moisture
- Braden Scale: Moisture subscale (rarely moist → constantly moist)
Prevention Strategies
- Structured incontinence care regimen — timed toileting, scheduled brief checks
- Moisture barrier cream/ointment (zinc oxide, petrolatum) after each incontinence episode
- Fecal management system for liquid stool if warranted
- Absorbent, moisture-wicking underpads and briefs
- Treat root cause of moisture (diuretics for diaphoresis, bowel regimen)
Friction
Braden: Friction and ShearMechanism: Friction occurs when skin moves against a surface — dragging a patient across bed linens. Friction removes superficial layers of skin, creating abrasions. Unlike pressure, friction damages the epidermis from the outside in. Friction is often paired with shear.
Assessment Focus
- Ability to lift or reposition without dragging across surface
- Existing skin abrasions over heels, elbows, occiput
- Agitated or confused patients who slide against bed rails or move restlessly
- Braden Scale: Friction and Shear subscale (no apparent problem / potential problem / problem)
- Spasticity or involuntary movements
Prevention Strategies
- Lift — never drag — patient during repositioning (use draw sheet, slider board)
- Apply transparent film or foam dressings to high-friction sites (heels, elbows)
- Heel protectors / heel lift devices to float heels
- Moisture-reducing products — wet skin has higher friction coefficient
- Silk-like (low-friction) bed linens or transfer sheets
Shear
Braden: Friction and ShearMechanism: Shear occurs when deeper tissue layers move while skin remains fixed — the skeleton slides forward while the skin stays against the surface. Shear stretches and tears blood vessels supplying the dermis and subcutaneous tissue. Elevating the head of bed >30 degrees causes significant sacral shear. DTPI is strongly associated with shear forces.
Assessment Focus
- Head of bed elevation consistently >30 degrees
- Sliding down in bed or chair (gravity-induced shear)
- Sacral or coccygeal skin integrity — highest shear-impact area
- Tone and spasticity (increased shear with spasms)
- Braden Scale: Friction and Shear subscale
Prevention Strategies
- Limit HOB elevation to 30 degrees or less when possible
- Use knee-break (fowler position) to prevent patient sliding down
- Reposition patient to foot of bed before raising HOB
- Use low-shear support surfaces
- Protect coccyx/sacrum with pressure-redistributing foam or specialty cushion
Diabetes Mellitus
Braden: Sensory Perception (neuropathy) + NutritionMechanism: Hyperglycemia impairs all phases of wound healing: neuropathy → loss of protective sensation (patient cannot feel pressure pain signals), autonomic neuropathy → impaired sweating → dry cracked skin, motor neuropathy → foot deformities, peripheral arterial disease → ischemia, and immune impairment (neutrophil dysfunction).
Assessment Focus
- Glucose control: HbA1c, current blood glucose (target <180 mg/dL hospitalized)
- Neuropathy assessment: Semmes-Weinstein 10g monofilament test; protective sensation
- Peripheral pulses and capillary refill; ABI if arterial insufficiency suspected
- Foot inspection: calluses, fissures, blisters, ulcers, deformities
- Footwear assessment — poorly fitting shoes cause DFU
Prevention Strategies
- Glycemic control optimization — key modifiable risk factor for wound healing
- Daily structured foot inspection (patient self-care or nursing)
- Therapeutic footwear to offload pressure points
- Monofilament testing annually (or per clinical protocol) to identify neuropathy
- Patient education: never walk barefoot; report any foot wounds immediately
Poor Perfusion
Braden: Sensory Perception (indirectly)Mechanism: Tissue perfusion delivers oxygen and nutrients required for cellular survival and healing. Peripheral arterial disease, congestive heart failure, hypovolemia, anemia, and sepsis all reduce oxygen delivery to tissues. Without adequate oxygen, even brief pressure cannot be tolerated and healing cannot occur.
Assessment Focus
- Peripheral pulses: posterior tibial and dorsalis pedis (grade 0–4+)
- Capillary refill (normal <2 seconds)
- Skin color, temperature, and texture changes in extremities
- Ankle-brachial index (ABI) — normal 1.0–1.4; ≤0.9 = PAD; >1.4 = calcified/noncompressible vessels
- Hemoglobin and hematocrit (anemia impairs O2 delivery)
- Edema (venous insufficiency) — impairs healing despite adequate arterial inflow
Prevention Strategies
- Optimize blood pressure and cardiac output (hemodynamic stability)
- Treat anemia if present and clinically significant
- Smoking cessation — vasoconstrictive and carboxyhemoglobin effects
- Compression therapy for venous insufficiency (if arterial supply is adequate — check ABI first)
- Vascular surgery consult if significant PAD identified (ABI <0.5 or non-healing wound)
Related Resources
Standards & sources
Fact-checked Jun 21, 2026This page is written to align with NPIAP / Braden Scale / WOCN Clinical Guidelines. It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →