Pressure Injuries Lecture Notes

Flashcards on Pressure Injuries

Preferred term over pressure/decubitus ulcer or bedsore, caused by unrelieved prolonged pressure over a bony prominence.

Pressure Injury

Highest incidence in elderly patients with femoral neck fractures (66%), quadriplegic patients (60%), ICU patients (33%), and bed-bound hospital patients (10-15%).

Epidemiology of Pressure Injuries

Sacrum (28-36%), Heel (23-30%), Ischial tuberosity (17-20%), Trochanter (20%). Other sites include occipital region, malleoli, spine, shoulder/scapula.

Common Locations of Pressure Injuries

Prolonged pressure leads to increased interstitial pressure greater than capillary pressure, causing occlusion of small vessels, anoxia, accumulation of toxic metabolites, edema, inflammation, tissue ischemia, and necrosis.

Pathophysiology of Pressure Injuries

Mechanical force per unit area perpendicular to plan, causing tissue deformation, mechanical damage, and blockage of vessels leading to deep necrosis.

Pressure (Extrinsic Risk Factor)

Mechanical stress parallel to a plane, compressing muscle perforators to the skin and causing ischemic superficial necrosis (e.g., when the head of a bed is raised).

Shear (Extrinsic Risk Factor)

Resistance to movement between two surfaces, resulting in the loss of the outermost skin layer and increased water loss, often incurred during patient transfers.

Friction (Extrinsic Risk Factor)

Often the result of incontinence, leading to skin maceration and breakdown.

Moisture (Extrinsic Risk Factor)

Loss of protective reflexes or voluntary movements to off-load pressure/ coma.

Cognitive Deficit/Altered Consciousness (Intrinsic Risk Factor)

Inability to experience discomfort from prolonged sitting or other positions, leading to tissue ischemia.

Sensory Loss (Intrinsic Risk Factor)

A scale measuring the pressure injury risk using 6 domains: sensory perception, moisture, activity, mobility, nutrition, friction & shear. Lower scores indicate increased risk.

Braden Scale

Non-blanchable erythema of intact skin. Can be difficult to detect in dark-skinned patients.

Stage I Pressure Injury

Partial thickness skin loss with exposed dermis, presenting as a blister, abrasion, or shallow open ulcer.

Stage II Pressure Injury

Full-thickness tissue loss down to the hypodermis. Necrosis, black & dry patch are present.

Stage III Pressure Injury

Full thickness skin and tissue loss with exposed fascia, muscle, tendon, ligament, cartilage, or bone.

Stage IV Pressure Injury

Tissue tolerates increased pressure if interspersed with pressure-free periods.Seated patients must be lifted for 10 seconds every 10 minutes. Supine patients must be turned every 2 hours

Kosiak’s principle

Proper skin care, pressure dispersion (padding), pressure-relief behavior, support surfaces, proper positioning, incontinence management, proper nutrition, and optimizing underlying medical comorbidities.

Prevention of Pressure Injuries

Look for signs of local cellulitis and use topical antimicrobial agents: Sylvadens (Flamazine), Sulfamylon (mafenide)

Local Infection Treatment for Pressure Injuries

Systemic infection may exacerbate pressure injury. Rule out other sources: urinary tract infection or respiratory tract in case of fever.

Systemic Infection Considerations for Pressure Injuries

Antibiotherapy and surgery (debridement) are implemented for osteomyelitis.

Osteomyelitis Treatment

Debridement of all devitalized tissue with complete excision of pseudo-bursa and osteotomy of all devitalized or infected bone; secondary healing, topical creams, NPWT, closure of the wound

Surgical Treatment

Application of foam sponge or gauze covered by adhesive dressing applied to vacuum device provides constant - pressure (-50 to -175mmHg). Dressings every 48-72 hours.

Negative Pressure Wound Therapy (NPWT)

Direct contact with blood vessels, necrotic or infected wounds, or on denuded bone.

Contraindications of Negative Pressure Wound Therapy (NPWT)

Speeds overall collagen synthesis and rate of wound closure by offloading mechanical tension on wound. Reduces presence of inflammatory mediators. Promotes local wound blood flow and angiogenesis. Maintains moist wound environment and reduces edema

Mechanism of action of Negative Pressure Wound Therapy (NPWT)

Adjunct dressing to serve as bolster for skin grafts. Provides exudative management for draining wounds and wound care regimen is less frequent for patients.

Advantages for Negative Pressure Wound Therapy (NPWT)

Cost of device, pain or discomfort with dressing changes, peri-wound irritation secondary to adhesive tape.

Disadvantages for Negative Pressure Wound Therapy (NPWT)