# Pressure Injury Prevention and Management in SCI

## Overview
Pressure injuries (formerly "pressure ulcers" or "decubitus ulcers") are among the most common and costly complications of SCI. Lifetime incidence: 50-80% of SCI patients will develop at least one pressure injury. Prevalence at any given time: 25-30%. Leading cause of rehospitalization after SCI.

Associated with increased morbidity, mortality, decreased quality of life, and enormous healthcare costs. Annual cost in the US exceeds $11 billion for pressure injury care across all populations.

## Pathophysiology
Sustained pressure exceeding capillary closing pressure (~32 mmHg) causes tissue ischemia. Four key extrinsic factors: **Pressure**: perpendicular force compressing tissue between bone and support surface. **Shear**: parallel force causing tissue layers to slide (e.g., sliding down in bed).

**Friction**: resistance to movement across a surface (skin abrasion). **Moisture**: maceration weakens skin integrity (incontinence, perspiration). Intrinsic factors: malnutrition, anemia, diabetes, smoking, aging, impaired sensation, immobility. Deep tissue injury may occur before surface changes are visible (injury develops from deep to superficial). Muscle tissue is more susceptible to pressure damage than skin.

<image>Pathophysiology of pressure injury formation showing tissue layers, pressure distribution, and ischemic cascade</image>

## Risk Assessment
Braden Scale: most widely used risk assessment tool. Six subscales: sensory perception, moisture, activity, mobility, nutrition, friction/shear. Score range: 6-23 (lower = higher risk). At risk: ≤ 18; High risk: ≤ 14; Very high risk: ≤ 12.

SCI-specific risk factors: Complete injury > incomplete. Level of injury (cervical/thoracic > lumbar). Duration of injury.

Prior pressure injury history (strongest predictor of recurrence). Smoking, diabetes, malnutrition. Depression and substance abuse. Inadequate equipment (wheelchair cushion, mattress).

## Pressure Injury Staging (NPUAP/EPUAP)

### Stage 1
Intact skin with non-blanchable erythema. May appear differently in darkly pigmented skin (warmth, induration, discoloration). Painful in sensate individuals (not applicable in most SCI).

### Stage 2
Partial-thickness skin loss involving epidermis and/or dermis. Shallow open ulcer with red-pink wound bed. May present as intact or ruptured serum-filled blister. NOT a skin tear, tape burn, or moisture-associated skin damage.

### Stage 3
Full-thickness skin loss extending into subcutaneous tissue. Subcutaneous fat may be visible. Bone, tendon, and muscle NOT exposed. May include undermining and tunneling.

### Stage 4
Full-thickness tissue loss with exposed bone, tendon, or muscle. Often includes undermining and tunneling. Osteomyelitis risk is significant. May extend into joint capsule.

### Unstageable
Full-thickness tissue loss with wound base obscured by slough (yellow/tan) or eschar (black/brown). Cannot be staged until slough/eschar is removed. Exception: stable eschar on heels should not be removed.

### Deep Tissue Pressure Injury (DTPI)
Intact or non-intact skin with localized area of persistent non-blanchable deep red, maroon, or purple discoloration. May present as blood-filled blister. Represents damage to underlying tissue from pressure/shear. May rapidly evolve to full-thickness injury.

| Stage | Tissue Involvement | Wound Bed Appearance | Key Features |
|-------|-------------------|---------------------|--------------|
| 1 | Intact skin | Non-blanchable erythema | Warmth, induration; reversible |
| 2 | Epidermis/dermis | Shallow, red-pink base or blister | Partial thickness; no slough |
| 3 | Subcutaneous tissue | Fat visible; may tunnel | Full thickness; no bone/tendon exposed |
| 4 | Bone, tendon, or muscle exposed | Deep, may tunnel extensively | Osteomyelitis risk |
| Unstageable | Full thickness | Obscured by slough/eschar | Must debride to stage |
| DTPI | Deep tissue (intact/non-intact skin) | Purple/maroon discoloration | May rapidly evolve |

<image>NPUAP pressure injury staging system from Stage 1 through Stage 4 with deep tissue injury</image>

## Common Locations in SCI
Sacrum/coccyx (most common overall, especially in bed-bound). Ischial tuberosities (most common in wheelchair users). Greater trochanters (side-lying). Heels (supine positioning). Occiput (cervical SCI, halo vest). Malleoli, elbows, scapulae (less common).

## Prevention Strategies

### Skin Inspection
Full-body skin check at least twice daily. Use mirror for areas patient cannot visualize. Educate patient and caregivers on inspection technique. Pay special attention to bony prominences and areas under devices.

### Pressure Redistribution
**In bed**: Pressure-redistributing support surface (Group 1, 2, or 3). Repositioning every 2 hours. Avoid positioning directly on trochanters (30-degree lateral tilt).

Elevate heels off the bed surface. Limit head-of-bed elevation to < 30 degrees when possible (reduces sacral shear). **In wheelchair**: Appropriate pressure-relieving cushion (air, gel, foam, or combination).

Pressure mapping to optimize cushion selection and seating. Weight shifts every 15-30 minutes (forward lean, lateral lean, or wheelchair tilt/recline). Proper wheelchair fit and positioning.

### Nutrition
Caloric intake adequate for wound healing. Protein goal: 1.25-1.5 g/kg/day for at-risk patients; up to 2 g/kg/day for active wounds. Monitor serum albumin (goal > 3.5 g/dL) and prealbumin (goal > 15 mg/dL). Vitamin C (500 mg BID) and zinc (220 mg daily) supplementation for wound healing. Registered dietitian consultation.

### Moisture Management
Effective bladder and bowel management program. Moisture barrier creams for perineal skin protection. Prompt cleaning after incontinence episodes. Manage excessive perspiration.

### Education
Patient and caregiver education is the foundation of prevention. Skin check technique, weight shift schedule, nutrition, equipment maintenance. Behavioral factors: smoking cessation, avoiding alcohol excess. Recognize early warning signs.

## Wound Management

### Assessment
Location, stage, size (length x width x depth). Wound bed description (granulation, slough, eschar, necrotic tissue). Periwound skin condition. Undermining and tunneling (document clock position and depth).

Exudate (amount, type, odor). Signs of infection (erythema, warmth, edema, purulent drainage, foul odor). Photography for serial comparison.

### Conservative Management
**Offloading**: complete pressure elimination from wound site. **Debridement**: sharp, enzymatic (collagenase), autolytic, or mechanical. **Wound bed preparation**: maintain moist wound healing environment. **Dressing selection** by wound characteristics: 
Dry wound: hydrogel. Moderate exudate: foam, hydrofiber. Heavy exudate: alginate, negative pressure wound therapy. Infected/biofilm: antimicrobial dressings (silver, cadexomer iodine).

Necrotic: enzymatic debriding agents. **Negative pressure wound therapy (NPWT/VAC)**: promotes granulation tissue in Stage 3-4 wounds. Nutritional optimization throughout healing.

### Surgical Management
Indications: Stage 3-4 wounds failing conservative management, osteomyelitis. Surgical options: Direct closure (small wounds). Skin grafting.

Musculocutaneous flap closure (most common for large SCI pressure injuries). Gluteus maximus flap (sacral). Posterior thigh flap/biceps femoris (ischial). Tensor fascia lata flap (trochanteric).

Post-operative management: strict bed rest on flap-free surface for 2-6 weeks, gradual progressive sitting protocol. Recurrence rate: 25-80% even after surgical repair.

<image>Musculocutaneous flap options for surgical closure of pressure injuries at sacral, ischial, and trochanteric sites</image>

### Osteomyelitis Evaluation
Suspect in non-healing Stage 3-4 wounds overlying bone. Probe-to-bone test: positive test has high positive predictive value. ESR and CRP: elevated but nonspecific. MRI: imaging modality of choice (sensitivity ~90%).

Bone biopsy with culture: gold standard for diagnosis. Treatment: surgical debridement + prolonged antibiotics (6+ weeks).

## Clinical Pearls
Prior pressure injury is the strongest predictor of future pressure injury - these patients need intensified surveillance. In darkly pigmented skin, Stage 1 pressure injuries may not show visible erythema - palpate for warmth, induration, and bogginess. Ischial pressure injuries in wheelchair users almost always indicate inadequate cushion, improper seating, or poor weight-shift compliance. Heel pressure injuries are among the most preventable - elevating heels off the bed surface with a pillow is a simple, effective intervention. A wound that fails to show 20-40% reduction in size over 2-4 weeks of appropriate management should prompt reassessment of treatment plan, nutrition, offloading, and infection evaluation.

<image>Wheelchair pressure mapping demonstrating ischial pressure distribution with different cushion types</image>

## References
- European Pressure Ulcer Advisory Panel, National Pressure Injury Advisory Panel, Pan Pacific Pressure Injury Alliance. Prevention and Treatment of Pressure Ulcers/Injuries: Clinical Practice Guideline. 3rd ed. 2019.
- Consortium for Spinal Cord Medicine. Pressure ulcer prevention and treatment following SCI: a clinical practice guideline. 2nd ed. 2014.
- Gélis A, et al. Pressure ulcer risk factors in persons with SCI. Spinal Cord. 2009;47(9):651-661.
- Kruger EA, et al. Comprehensive management of pressure ulcers in spinal cord injury. J Spinal Cord Med. 2013;36(6):572-585.
- Cifu DX, et al. Braddom's Physical Medicine and Rehabilitation. 6th ed. Elsevier; 2020.