3.2 Wound Care, Pressure Injury Staging & Healing

Wound Care, Pressure Injury Staging & Healing

Preserving skin integrity and facilitating tissue repair are fundamental registered nursing responsibilities. Pressure injuries are localized skin and soft-tissue damage caused by intense or prolonged pressure, alone or combined with shear; friction and moisture increase tissue vulnerability. Understanding standardized risk stratification, anatomical staging systems, physiological healing phases, and modern dressing chemistry is essential for optimizing clinical outcomes.

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Pressure Injury Pathophysiology & Risk Assessment: The Braden Scale

Prolonged pressure and shear deform tissue and impair local microvascular perfusion. When microvascular perfusion is occluded for prolonged periods, localized cellular ischemia, anoxia, accumulation of metabolic waste products, and tissue necrosis ensue. Subsequent reperfusion generates reactive oxygen species, compounding cellular death.

• High-Risk Bony Prominences: Sacrum, ischial tuberosities, greater trochanters, calcaneus (heels), occiput, lateral malleoli, and scapulae.
• Medical Device-Related Pressure Injuries (MDRPI): Result from the use of devices designed for diagnostic or therapeutic purposes (endotracheal tubes, tracheostomy ties, non-invasive ventilation masks, nasogastric tubes, urinary catheters, cervical collars). Skin under devices must be inspected at least twice daily.

The Braden Scale for Predicting Pressure Sore Risk

The Braden Scale is the most widely validated clinical risk assessment instrument in adult acute and long-term care settings. It evaluates six physiological and functional subscales:

1. Sensory Perception (1 to 4): Ability to respond meaningfully to pressure-related discomfort (1 = completely limited, 4 = no impairment).
2. Moisture (1 to 4): Degree to which skin is exposed to moisture from perspiration, urine, or feces (1 = constantly moist, 4 = rarely moist).
3. Activity (1 to 4): Degree of physical activity (1 = bedfast, 4 = walks frequently).
4. Mobility (1 to 4): Ability to adjust and control body position independently (1 = completely immobile, 4 = no limitations).
5. Nutrition (1 to 4): Usual food intake pattern (1 = very poor, 4 = excellent).
6. Friction and Shear (1 to 3): Mechanical tissue deformation during movement (1 = problem, 2 = potential problem, 3 = no apparent problem).

Total Braden scores range from 6 to 23. Lower scores indicate higher clinical vulnerability:

• Score ≤18: Threshold for clinical risk in adult acute care
• 15 to 18: Mild risk
• 13 to 14: Moderate risk
• 10 to 12: High risk
• ≤9: Very high risk

Evidence-Based Nursing Interventions by Subscale Deficit

• Mobility / Activity Deficits:
  • Individualize bed and chair repositioning to mobility, skin response, comfort and support surface. On an appropriate pressure-redistributing mattress, two- or three-hour turns suit many at-risk patients; reassess the schedule as condition changes.
  • Maintain a 30-degree lateral tilted position using positioning wedges, avoiding direct 90-degree trochanteric weight-bearing.
  • Float the heels completely off the mattress surface by placing longitudinal pillows beneath the calves, ensuring the calcaneus remains entirely suspended without pressure.
  • Utilize specialized dynamic pressure-redistributing support surfaces (alternating-pressure air mattresses, low-air-loss beds).
• Moisture Management:
  • Cleanse skin promptly after incontinent episodes using pH-balanced, no-rinse perineal cleansers; avoid vigorous scrubbing.
  • Apply silicone- or dimethicone-based moisture barrier creams or zinc oxide ointments to protect against incontinence-associated dermatitis (IAD).
  • Place breathable underpads; never use multiple layered disposable pads, which trap heat and moisture.
• Friction & Shear Mitigation:
  • Keep the head of the bed elevated to ≤30 degrees (except during meals or when clinically indicated for aspiration precautions) to minimize gravitational pelvic slide.
  • Utilize friction-reducing slide sheets, ceiling lifts, or hover air-transfer devices during patient transfers and repositioning.
  • Apply prophylactic multi-layered silicone sacral foam dressings for high-risk patients.
• Nutritional Support:
  • Assess nutritional needs with the dietitian and provide the indicated high-protein diet or supplements; a common healing target is 1.25 to 1.5 grams of protein/kg body weight/day.
  • Supplement with L-arginine, zinc, and ascorbic acid (vitamin C) to promote collagen cross-linking.

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National Pressure Injury Advisory Panel (NPIAP) Staging System

The NPIAP staging classification categorizes pressure injuries based on the maximum anatomical depth of visible or palpable tissue destruction. Once staged, pressure injuries are tracked through healing (e.g., "healing Stage 4 pressure injury"); they are never reverse-staged (a Stage 4 does not become a Stage 3 as it fills with granulation tissue).

Stage 1 Pressure Injury: Non-Blanchable Erythema of Intact Skin

• Anatomical Depth: Epidermis remains completely intact.
• Presentation: Localized area of persistent non-blanchable erythema over a bony prominence. When digital pressure is applied for 3 seconds, the redness does not blanch (turn white).
• Darker Skin Tones: Non-blanchable erythema may be difficult to see. Compare the area with adjacent skin and assess pain, temperature and firmness. Purple or maroon discoloration is not part of Stage 1 and may indicate deep tissue pressure injury.

Stage 2 Pressure Injury: Partial-Thickness Skin Loss with Exposed Dermis

• Anatomical Depth: Loss of epidermis extending into the superficial papillary dermis.
• Presentation: The wound bed is viable, pink or red, and moist. Commonly presents as an intact or ruptured serum-filled blister, or a shallow, moist open ulcer.
• Diagnostic Boundaries: Subcutaneous adipose tissue, granulation tissue, slough, and eschar are completely absent. Must not be confused with moisture-associated skin damage (MASD), intertrigo, adhesive tape burns, or traumatic skin tears.

Stage 3 Pressure Injury: Full-Thickness Skin Loss

• Anatomical Depth: Full-thickness loss extending through the epidermis and dermis into the hypodermis (subcutaneous layer).
• Presentation: Subcutaneous adipose (fat) tissue is visible. Granulation tissue (beefy red, cobblestone appearance) and epibole (rolled wound edges) are frequently present. Slough and/or eschar may be visible on the wound surface, but they do not obscure the depth of tissue loss.
• Undermining & Tunneling: May occur beneath the intact skin margins.
• Critical Diagnostic Boundary: Fascia, muscle, tendon, ligament, cartilage, and bone are NOT exposed or directly palpable.

Stage 4 Pressure Injury: Full-Thickness Skin and Tissue Loss

• Anatomical Depth: Complete tissue destruction extending beyond the subcutaneous layer.
• Presentation: Directly exposed or palpable fascia, muscle, tendon, ligament, cartilage, or bone. Slough and eschar are commonly present on portions of the wound bed. Epibole, deep undermining, and extensive sinus tract tunneling frequently occur.
• Clinical Risks: Extreme risk of contiguous osteomyelitis, bacteremia, septic arthritis, and systemic sepsis.

Unstageable Pressure Injury: Obscured Full-Thickness Skin and Tissue Loss

• Anatomical Depth: True full-thickness loss (Stage 3 or Stage 4), but anatomical depth cannot be confirmed.
• Presentation: Slough or eschar prevents confirmation of the full extent of tissue loss. No fixed percentage of wound coverage defines unstageable injury. If the obstructing tissue is appropriately removed, Stage 3 or 4 may be revealed.
• Stable Eschar on Heels or Ischemic Limbs: Stable eschar is dry, adherent and intact, without erythema or fluctuance. Do not soften or remove stable eschar on a heel or ischemic limb. Protect and offload the area, assess perfusion and monitor for infection. New drainage, fluctuance, erythema or systemic illness requires prompt medical/wound or vascular review; do not treat infected or unstable tissue as a protective cover.

Deep Tissue Pressure Injury (DTPI): Persistent Non-Blanchable Deep Red, Maroon, or Purple Discoloration

• Anatomical Depth: Deep soft-tissue injury initiated at the muscle-bone interface secondary to severe mechanical shear and compression.
• Presentation: Intact or non-intact skin with localized, persistent, non-blanchable deep red, maroon, or purple discoloration, or epidermal separation revealing a dark wound bed or blood-filled blister.
• Clinical Course: May evolve rapidly to expose the true extent of deep tissue destruction (rapidly converting into a full-thickness Stage 3 or Stage 4 ulcer), or may resolve without significant tissue loss if pressure is promptly eliminated.

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Wound Healing Physiology & Closure Intentions

Cutaneous wound healing proceeds through four synchronized, overlapping physiological phases orchestrated by platelets, leukocytes, fibroblasts, and endothelial cells.

Phases of Wound Healing

1. Hemostasis Phase (Immediate Onset):
   • Microvascular injury triggers immediate transient vasoconstriction followed by platelet adhesion to exposed subendothelial collagen.
   • Platelets form a plug at the injury site; fibrin reinforces it into a clot that helps arrest hemorrhage.
   • Platelets release essential chemotactic cytokines and growth factors, including Platelet-Derived Growth Factor (PDGF) and Transforming Growth Factor-beta (TGF-β), to recruit inflammatory cells.
2. Inflammatory Phase (Day 1 to Day 4):
   • Local vasodilation increases capillary permeability, producing classic signs of erythema, heat, edema, and pain.
   • Neutrophils infiltrate within the first 24 hours to phagocytose contaminating bacteria and necrotic cellular debris via reactive oxygen species and proteases.
   • By 48 to 72 hours, circulating monocytes migrate into the tissue and differentiate into tissue macrophages. Macrophages are the master orchestrators of healing: they perform extensive phagocytosis, clear apoptotic neutrophils, secrete matrix metalloproteinases (MMPs), and release vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) to initiate the proliferative phase.
3. Proliferative Phase (Day 4 to Day 21):
   • Angiogenesis: Endothelial cells sprout new microvascular capillaries, forming vibrant, beefy red, highly vascularized granulation tissue.
   • Fibroplasia: Fibroblasts synthesize extracellular matrix components, predominantly Type III collagen and proteoglycans.
   • Wound Contraction: Specialized myofibroblasts containing alpha-smooth muscle actin anchor to wound margins and pull tissue edges inward.
   • Epithelialization: Keratinocytes at wound margins detach, migrate across the moist wound surface, proliferate, and restore epidermal continuity.
4. Maturation / Remodeling Phase (Day 21 up to 2 Years):
   • Type III collagen is progressively degraded by matrix metalloproteinases and replaced by organized, cross-linked Type I collagen oriented along mechanical tension lines.
   • Microvascular density regresses, transforming pink granulation into a pale, avascular, flat scar.
   • Tensile Strength: Scar strength increases during remodeling, reaching a maximum of approximately 80% of pre-injury strength. It does not regain the full strength or normal accessory structures, such as hair follicles and sweat glands, of uninjured skin.

Surgical & Clinical Healing Intentions

• Primary Intention: Clean surgical incisions where wound margins are closely approximated using sutures, staples, or tissue adhesives. Minimal tissue loss, minimal granulation required, rapid re-epithelialization within 48 to 72 hours, resulting in a fine, linear scar.
• Secondary Intention: Wounds involving significant tissue loss, irregular margins, or gross contamination (e.g., deep pressure injuries, debrided abscess cavities, venous ulcers). Margins cannot be approximated. The wound must heal from the base upward through extensive granulation tissue formation, wound contraction, and epithelial migration. Associated with prolonged healing time, higher infection risk, and substantial scar formation.
• Tertiary Intention (Delayed Primary Closure): Heavily contaminated, infected, or severely edematous wounds intentionally left open for 3 to 7 days to allow aggressive drainage, debridement, or antimicrobial therapy. Once the bacterial bioburden is controlled, edema resolves, and healthy granulation tissue appears, the wound margins are surgically approximated and closed with sutures or staples.

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Evidence-Based Dressing Selection & Moisture Balance Principles

Modern wound care is governed by the principle of moist wound healing (established by Winter in 1962). A moisture-balanced wound bed supports epithelial migration and autolytic removal of devitalized tissue. However, excessive moisture macerates surrounding intact peri-wound skin, while insufficient moisture causes tissue desiccation and cellular death.

Modern Dressing Classifications

• Hydrocolloids (e.g., Carboxymethylcellulose wafers):
  • Mechanism: Gel-forming polymers bonded to a semi-permeable film. Interacts with wound fluid to form a soft hydrophilic gel, promoting autolytic debridement and thermal insulation.
  • Indications: Partial-thickness injuries (Stage 2 pressure injuries, clean superficial abrasions) with low to moderate exudate.
  • Contraindications: Heavily exuding wounds, deep cavity wounds, anaerobic infections, and fragile surrounding skin.
• Calcium Alginates (e.g., Seaweed-derived fibers):
  • Mechanism: Calcium ions within non-woven alginate fibers exchange with sodium ions in wound exudate, transforming the fibers into an absorbent sodium alginate gel. Provides high absorption for exudate management; change according to saturation and product instructions.
  • Indications: Moderately to heavily exuding wounds, cavity packing, and bleeding wound beds (provides mild hemostasis).
  • Contraindications: Dry necrotic eschar, minimal drainage (causes wound bed desiccation and fiber adherence). Requires secondary cover dressing.
• Hydrogels (Amorphous gels and impregnated sheets):
  • Mechanism: Glycerin- and water-based polymers with high water content. Donates moisture to dry, devitalized wound beds to rehydrate necrotic slough and eschar, facilitating painless autolytic debridement.
  • Indications: Selected dry, healable wounds that need added moisture, including dry pressure injuries, after assessment of perfusion and tissue status. Do not use hydrogel to soften stable heel or ischemic-limb eschar.
  • Contraindications: Heavily exuding or infected cavitary wounds.
• Transparent Polyurethane Films:
  • Mechanism: Semi-permeable adhesive membranes that permit oxygen and moisture vapor transmission while acting as an impermeable barrier to water, urine, and bacteria.
  • Indications: Stage 1 pressure injury protection, intravenous catheter dressing security, superficial non-draining tears.
  • Limitations: Films do not absorb fluid and are unsuitable as the sole primary dressing for moderate or heavy exudate; trapped fluid can macerate surrounding skin.
• Polyurethane Foams:
  • Mechanism: Hydrophilic polyurethane foam pads with semi-permeable backing. Handles high exudate volumes, provides mechanical cushioning over bony prominences, and maintains thermal insulation.
  • Indications: Stage 2, 3, and 4 pressure injuries with moderate to heavy exudate, skin tears, and donor sites.
  • Contraindications: Dry, non-draining wounds or hard black eschar.

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Clinical Reference: NPIAP Staging, Presentation & Dressing Guidelines