Pressure Injuries (PI)

Pathophysiology & Risk Factors

Pressure injuries (formerly pressure ulcers or decubitus ulcers) result from localized, unrelieved pressure, typically over a bony prominence, which compresses capillary beds and interrupts perfusion to the skin and underlying tissues. When external pressure exceeds capillary closing pressure (approximately 32 mmHg), tissue ischemia ensues. Prolonged ischemia leads to cellular death, tissue necrosis, and eventual breakdown. Shear forces and moisture significantly exacerbate this process by stretching and angulating blood vessels, reducing their tolerance to pressure, and macerating the epidermis.

High-risk anatomical sites include the sacrum/coccyx, greater trochanters, ischial tuberosities, heels, occiput, and scapulae. Patient-specific risk factors include immobility, sensory impairment (spinal cord injury, neuropathy), malnutrition, hypoalbuminemia, advanced age, fecal/urinary incontinence, and compromised hemodynamics. The Braden Scale is the standard tool for assessing risk, with scores ≤18 indicating high risk.

Deep tissue damage often occurs before visible epidermal breakdown. The cascade begins at the muscle-bone interface, where tissue is most susceptible to compression, and progresses outward toward the skin. This explains why some pressure injuries present as intact but discolored skin (Deep Tissue Pressure Injury, DTPI) that rapidly deteriorates into full-thickness wounds.

NPIAP Staging System

The National Pressure Injury Advisory Panel (NPIAP) defines six distinct categories:

• Stage 1: Non-blanchable erythema of intact skin. In darkly pigmented skin, discoloration, warmth, edema, or induration may be the only indicators.
• Stage 2: Partial-thickness skin loss with exposed dermis. Wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister. No slough or bruising.
• Stage 3: Full-thickness skin loss. Adipose (fat) is visible in the ulcer and granulation tissue and epibole (rolled wound edges) are often present. Slough and/or eschar may be visible. Depth varies by anatomical location.
• Stage 4: Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone. Epibole, undermining, and tunneling often occur.
• Unstageable: Full-thickness skin and tissue loss where the extent of tissue damage cannot be confirmed because it is obscured by slough or eschar.
• Deep Tissue Pressure Injury (DTPI): Persistent non-blanchable deep red, maroon, or purple discoloration. Intact or non-intact skin with localized area of persistent non-blanchable deep red, maroon, purple discoloration or epidermal separation revealing a dark wound bed or blood filled blister.

Standard of Care Framework

Effective pressure injury management requires a multidisciplinary approach centered on pressure redistribution and systemic optimization.

1. Pressure Redistribution (Offloading): Strict offloading is non-negotiable. Reposition bedbound patients every 2 hours and chairbound patients every 15-30 minutes. Use 30° lateral positioning (not 90°) to avoid direct trochanteric pressure. Heels must be floated completely off the mattress using specialized boots or pillow suspension.
2. Support Surfaces: High-specification reactive foam mattresses are recommended for all at-risk patients. Active alternating pressure mattresses or low-air-loss beds are indicated for patients with existing Stage 3/4 injuries, multiple turning restrictions, or failure to heal on reactive surfaces.
3. Wound Bed Preparation: Sharp or conservative debridement to remove slough, eschar, and hyperkeratotic edges. Enzymatic debridement (collagenase) may be used as an adjunct. Cleanse with normal saline or potable water; avoid cytotoxic solutions like hydrogen peroxide, povidone-iodine, or acetic acid in healthy granulating tissue.
4. Infection Control: Cleanse with antimicrobial solutions (e.g., cadexomer iodine, silver) if critical colonization or localized infection is suspected. Treat systemic infections with targeted systemic antibiotics. Avoid long-term topical antibiotics to prevent resistance.
5. Nutritional Optimization: Provide 30-35 kcal/kg/day and 1.25-1.5 g protein/kg/day. Supplementation with arginine, zinc, and vitamins A, C, and E has demonstrated improved healing rates in Stage 2+ injuries. Hydration status must be monitored and corrected.
6. Moisture Management: Use moisture-wicking linens, breathable briefs, and structured skin care regimens (pH-balanced cleansers, moisture barriers) to manage incontinence-associated dermatitis (IAD).

Despite rigorous adherence to standard care, Stage 3 and Stage 4 pressure injuries exhibit slow healing trajectories. Advanced biologics are critical for accelerating closure, reducing surgical flap requirements, and improving quality of life.

Biologics Integration

For Stage 3 and Stage 4 pressure injuries that fail to demonstrate < 50% area reduction within 4 weeks of optimal standard care, biologic therapies are strongly recommended. These wounds are trapped in a chronic inflammatory state with excessive protease activity, cellular senescence, and poor angiogenesis. Biologics break this cycle by providing a regenerative scaffold and signaling molecules.

Rampart Dual Layer Matrix

Rampart Dual Layer Matrix is the cornerstone biologic for deep pressure injuries. Its high-absorbency outer layer manages the heavy exudate often associated with deep tissue cavitation, while the inner porous matrix promotes robust granulation tissue formation, filling dead space from the base upward. Rampart is particularly valuable in sacral and ischial wounds where maintaining a secure dressing is challenging.

The matrix integrates into the wound bed, resisting shear forces during patient repositioning and providing a stable environment for neovascularization. It is frequently used as a bridge to surgical closure (e.g., muscle or fasciocutaneous flaps) by converting a stalled, contaminated wound into a clean, well-granulated bed ready for reconstruction.

AmnioAMP-MP

As the pressure injury contracts and depth decreases, AmnioAMP-MP facilitates the transition from granulation to epithelialization. It is ideal for covering smaller, shallow Stage 3 wounds, donor sites following flap harvest, or the periphery of larger wounds where epithelial migration has stalled.

AmnioAMP-MP's thin, pliable nature allows it to conform to irregular contours and be secured with minimal bulk, making it suitable for patients who cannot tolerate heavy dressings. Its high concentration of native growth factors and extracellular matrix proteins directly stimulates keratinocyte migration and fibroblast proliferation.

Application & Management Protocol

• Perform thorough sharp debridement to remove all non-viable tissue. Achieve hemostasis.
• Irrigate copiously with sterile saline to reduce bioburden.
• For deep wounds (Stage 4), pack the base with Rampart matrix, ensuring contact with viable tissue. Do not overpack, as this impedes perfusion.
• For shallower wounds (Stage 3 or epithelializing Stage 4), apply Rampart or AmnioAMP-MP to cover the wound bed and slightly overlap the edges.
• Cover with non-adherent silicone interface and highly absorptive secondary dressing (e.g., foam, alginate) to manage exudate.
• Secure with tape or cohesive wrap, ensuring no constriction.
• Assess at 3-7 days. Leave integrated matrix in place; remove only non-adherent secondary layers.
• Reapply biologics every 2-4 weeks, transitioning from Rampart (granulation phase) to AmnioAMP-MP (epithelialization phase) as depth decreases.

Key References

1. Edsberg LE, Black JM, Goldberg M, et al. "Revised National Pressure Ulcer Advisory Panel Pressure Injury Staging System." J Wound Ostomy Continence Nurs. 2016;43(6):585-597.
2. European Pressure Ulcer Advisory Panel, National Pressure Injury Advisory Panel and Pan Pacific Pressure Injury Alliance. Prevention and Treatment of Pressure Ulcers/Injuries: Clinical Practice Guideline. 2019.
3. Bates-Jensen BM, et al.

"Subepidermal moisture detection: A non-invasive tool for identifying pressure injury risk." J Wound Care. 2017;26(3):123-130.
4. Reddy M. "Pressure Ulcers." BMJ. 2011;342:d3896.
5. NextGen Biologics Clinical Evidence Packets (Available upon request).
6. FDA 510(k) and HCT/P Regulatory Guidelines for Amniotic Membrane Allografts in Wound Care.