Residency · Residency · Geriatrics

Pressure Injuries - Prevention and Management

Introduction

Pressure injuries, formerly known as pressure ulcers or decubitus ulcers, affect approximately 2.5 million patients annually in the United States and represent one of the most significant quality indicators in healthcare. Hospital-acquired prevalence ranges from 5 to 15 percent, rising to 10 to 25 percent in long-term care facilities and reaching 30 to 40 percent in intensive care units. Stage 3 and 4 pressure injuries are classified as "never events" by the Centers for Medicare and Medicaid Services and are not reimbursed as hospital-acquired conditions, reflecting the expectation that these injuries are largely preventable with appropriate care. The mortality associated with pressure injuries is 2 to 6 times higher than in matched controls without pressure injuries, and stage 4 sacral pressure injuries carry a 60 percent one-year mortality rate. The annual cost of pressure injury care in the United States is 9 to 11 billion dollars, with individual stage 4 wound treatment costing 125,000 to 150,000 dollars.

Pathophysiology

The primary mechanism of pressure injury development is sustained pressure exceeding capillary closing pressure, approximately 32 mmHg, which leads to tissue ischemia and ultimately cell death. Contributing biomechanical forces include shear, in which deeper tissue layers slide against superficial layers (as occurs when a patient slides down in bed), disrupting blood vessels at the tissue-bone interface; friction, which produces superficial epidermal damage from rubbing against bed linens or other surfaces; and moisture, which macerates the epidermis and weakens its protective barrier function, with incontinence, perspiration, and wound drainage being the primary sources.

Tissue tolerance to pressure is modified by nutritional status, tissue perfusion, oxygenation, sensory perception (which determines the patient's ability to perceive and respond to pressure-related discomfort), and the overall integrity of the skin and underlying tissues. A critically important concept is the inverted cone model of deep tissue injury, in which damage begins at the bone-muscle interface where pressure is highest and extends outward toward the skin surface. This means that the clinically visible injury on the skin surface may significantly underrepresent the extent of deep tissue damage. The time-pressure relationship dictates that higher pressures require less time to cause injury; interface pressures exceeding 60 mmHg sustained for more than one to two hours cause irreversible tissue damage.

Risk Assessment

Braden Scale (Most Widely Used)

The Braden Scale is the most widely validated risk assessment instrument, comprising six subscales each scored from 1 to 4 (except friction/shear, scored 1 to 3), yielding a total score from 6 to 23. The subscales assess sensory perception (the ability to respond to pressure-related discomfort), moisture exposure, activity level, mobility (the ability to change and control body position), nutritional status, and friction and shear forces. A total score of 18 or below indicates risk, 15 or below indicates moderate risk, 12 or below indicates high risk, and 9 or below indicates very high risk. Assessment should be performed on admission and at regular intervals thereafter (daily in acute care, weekly in long-term care, and with any significant change in condition). The Braden Scale has a sensitivity of 74 percent and specificity of 69 percent and should be combined with clinical judgment rather than relied upon in isolation.

Norton Scale

The Norton Scale assesses five subscales (physical condition, mental condition, activity, mobility, and incontinence), each scored 1 to 4, with a total score range of 5 to 20. A score of 14 or below indicates risk for pressure injury development.

Key Risk Factors

Immobility is the strongest modifiable risk factor for pressure injury development. Malnutrition (albumin below 3.5 g/dL, unintentional weight loss, inadequate caloric intake) impairs tissue repair and resistance to injury. Moisture exposure from urinary and fecal incontinence promotes skin maceration. Sensory impairment from neuropathy, spinal cord injury, or sedation eliminates the protective response to pressure-related discomfort. Advanced age produces skin atrophy, reduced subcutaneous tissue, and impaired perfusion. Medical comorbidities including diabetes, peripheral vascular disease, heart failure, renal failure, and COPD all increase susceptibility. Acute illness and critical care further elevate risk. Friction and shear forces, particularly during repositioning, contribute to injury. A history of prior pressure injury carries a 30 to 40 percent recurrence rate.

<image>A cross-sectional anatomical diagram showing the pathophysiology of pressure injury development. Show a patient lying supine on a hospital bed with a zoomed-in cross-section of tissue over the sacrum. The cross-section should show layers: epidermis, dermis, subcutaneous fat, muscle, and bone (sacrum). Illustrate the "inverted cone" model with pressure arrows from the bone-surface interface showing how deep tissue injury begins at the bone-muscle junction and extends outward. Show compressed blood vessels in the pressure zone with ischemic tissue (depicted in darker color). Include separate small diagrams showing shear force (tissue layers sliding), friction (epidermal abrasion), and moisture (maceration). Label capillary closing pressure (~32 mmHg) and show the pressure gradient from the bone surface to the external support surface. Include a time-pressure curve inset showing the relationship between applied pressure and duration needed to cause injury.</image>

Classification — NPUAP/EPUAP Staging System (2016 Updated)

Stage 1: Non-Blanchable Erythema

Stage 1 presents as intact skin with non-blanchable redness over a bony prominence. In darkly pigmented skin, visible blanching may not be apparent, and the clinician should look for changes in color, temperature, edema, or induration compared to surrounding tissue. Stage 1 injuries are fully reversible, typically resolving within 72 hours if pressure is adequately relieved.

Stage 2: Partial-Thickness Skin Loss

Stage 2 presents as a shallow open ulcer with a red or pink wound bed without slough, or as an intact or ruptured serum-filled blister. The injury does not extend into deeper tissue, and bone, tendon, and muscle are not exposed. This stage should not be used to describe skin tears, tape burns, moisture-associated skin damage, or incontinence-associated dermatitis, which have different etiologies and management approaches.

Stage 3: Full-Thickness Skin Loss

Stage 3 involves full-thickness skin loss with fat visible in the wound bed. Undermining and tunneling may be present. Bone, tendon, and muscle are not exposed or directly palpable. The depth varies significantly by anatomical location, appearing shallow over areas with thin subcutaneous tissue (nose, ear, occiput) and potentially very deep over areas with thick subcutaneous tissue (sacrum, buttock).

Stage 4: Full-Thickness Tissue Loss

Stage 4 involves full-thickness tissue loss with exposed bone, tendon, or muscle. Undermining, tunneling, and sinus tracts may be present. Necrotic tissue (slough or eschar) is frequently present. Osteomyelitis and sepsis are significant risks at this stage. The sacrum, heel, and ischium are the most common locations for stage 4 injuries.

Unstageable

Unstageable injuries involve full-thickness tissue loss with the wound base obscured by slough (yellow, tan, gray) or eschar (black, brown), preventing determination of the true wound depth until the non-viable tissue is removed. The critical exception is stable, dry eschar on the heel, which serves as a natural biological cover and should not be removed unless signs of infection develop.

Deep Tissue Pressure Injury (DTPI)

Deep tissue pressure injury presents as intact or non-intact skin with a persistent area of non-blanchable deep red, maroon, or purple discoloration, or as epidermal separation revealing a dark wound bed or blood-filled blister. It results from intense and prolonged pressure and shear at the bone-muscle interface and may evolve rapidly to full-thickness injury despite optimal treatment, representing an "unavoidable" progression in some cases. Deep tissue pressure injury must be distinguished from bruising, deep vein thrombosis, and calciphylaxis.

Mucosal Membrane Pressure Injury

Mucosal membrane pressure injuries develop at sites of medical device contact, including endotracheal tubes, nasogastric tubes, oxygen cannulae, urinary catheters, tracheostomy appliances, and orthopedic devices. These injuries cannot be staged using the standard classification system.

Prevention (Most Important Intervention)

Pressure Redistribution

Repositioning is the cornerstone of pressure injury prevention. Bed-bound patients should be repositioned every 2 hours and chair-bound patients every 1 hour. A 30-degree lateral tilt is preferred to avoid direct pressure on the trochanters. Heels should be elevated off the bed surface using pillows or dedicated heel suspension devices, as heels are the second most common site for pressure injuries. Head-of-bed elevation should be limited to 30 degrees or less when clinically possible to reduce sacral shear forces.

Support surfaces play a critical role in pressure redistribution. Reactive surfaces (constant low pressure) include foam mattresses, gel overlays, and air-fluidized mattresses. Active surfaces (alternating pressure) including alternating-pressure air mattresses have evidence for preventing stage 1 and 2 injuries. Low-air-loss and air-fluidized beds are indicated for high-risk patients or those with existing stage 3 or 4 injuries. Standard hospital mattresses are inadequate for at-risk patients. Pressure-redistributing chair cushions should be used with chair sitting limited to 2 hours and weight repositioned frequently. Ring cushions ("donuts") must not be used because they concentrate pressure at the edges.

Skin Care

Skin should be kept clean and dry using gentle cleansers with a pH of 5.5. Moisture barrier cream (dimethicone-based, zinc oxide, or petrolatum) should be applied for incontinence-associated moisture exposure. Aggressive rubbing should be avoided; skin should be patted dry. Daily skin inspection should be performed, focusing on bony prominences including the sacrum, heels, ischial tuberosities, trochanters, occiput, scapulae, and malleoli.

Nutrition

Nutritional screening using validated tools (MNA, SGA) should be performed in all at-risk patients. Caloric targets of 30 to 35 kcal/kg/day support wound healing. Protein targets of 1.25 to 1.5 g/kg/day provide the amino acid substrate necessary for tissue repair. Oral nutritional supplements reduce pressure injury incidence by 25 percent, as demonstrated in a Cochrane review. Micronutrient supplementation with vitamin C (500 mg twice daily) and zinc (220 mg daily) is commonly recommended if deficiency is present, though direct evidence is limited. Anemia should be corrected if significant.

Other Prevention Strategies

Continence management, moisture barriers, and absorbent products minimize moisture exposure. Draw sheets should be used for repositioning to reduce friction and shear (patients should never be dragged). Heel and elbow protectors provide targeted pressure relief. Perfusion should be optimized by avoiding unnecessary vasopressor use, treating heart failure, and optimizing oxygenation. Patient and caregiver education should cover skin inspection, repositioning schedules, and nutritional needs. Medical device-related pressure injury prevention requires assessment under and around all devices every shift, rotation of pulse oximeter probes, and securing tubes without creating localized pressure.

<image>An educational poster showing the NPUAP pressure injury staging system with clinical illustrations. Display six panels arranged in a grid, each showing a cross-sectional diagram of tissue layers alongside a clinical surface view. Stage 1: intact skin with non-blanchable erythema, cross-section showing compressed superficial vessels. Stage 2: partial-thickness loss with shallow wound or blister, cross-section showing epidermis/dermis disruption. Stage 3: full-thickness loss with visible fat, cross-section showing destruction through subcutaneous layer. Stage 4: full-thickness with exposed bone/tendon/muscle, cross-section showing destruction to bone level with potential osteomyelitis. Unstageable: wound covered by eschar/slough, cross-section showing unknown depth. DTPI: purple/maroon discoloration, cross-section showing deep tissue damage at bone-muscle interface with intact epidermis. Each panel should include the stage name, key features, common locations, and distinguishing characteristics. Use consistent color coding for tissue layers across all panels.</image>

Wound Management

Wound Assessment (Baseline and Serial)

Systematic wound assessment should document location, stage, dimensions (length by width by depth in centimeters), wound bed composition (percentage granulation tissue, slough, and necrotic or eschar tissue), wound edges (defined, rolled/epibole, undermining measured in centimeters at clock positions, tunneling), exudate (amount and type), periwound skin condition (maceration, erythema, induration, warmth), and pain at rest and with dressing changes. The PUSH tool (Pressure Ulcer Scale for Healing) provides a validated serial monitoring instrument combining area, exudate, and tissue type into a score from 0 to 17. Standardized photography at regular intervals documents healing trajectory.

Wound Bed Preparation — TIME Framework

The TIME framework structures wound bed preparation: Tissue management through debridement of non-viable tissue; Infection and inflammation control; Moisture balance through appropriate dressing selection; and Edge advancement assessment to monitor healing progress.

Debridement

Sharp or surgical debridement is the fastest method, performed by a trained provider, and is indicated when thick eschar is present, when cellulitis is advancing, or in the setting of sepsis. Autolytic debridement uses moisture-retentive dressings (hydrogels, hydrocolloids) to soften and liquefy necrotic tissue and is the slowest but least painful method. Enzymatic debridement with collagenase (Santyl) applied daily to the wound bed selectively degrades necrotic tissue and is compatible with most dressings. Mechanical debridement using wet-to-dry gauze is non-selective and painful and should be avoided; pulsed lavage with suction is better tolerated. Biological debridement using sterile maggots (Lucilia sericata) is highly selective and FDA-cleared but limited by patient and provider acceptance. The critical exception to the debridement principle is stable, dry, adherent eschar on the heel without signs of infection, which should be left intact and monitored closely.

Dressing Selection

Dressing selection should match the specific characteristics of the wound, following the moisture management principle of keeping the wound bed moist while keeping the periwound skin dry. Dry wounds benefit from hydrogels (which add moisture) and honey-based dressings. Moist wounds are managed with foam dressings and hydrofiber (Aquacel). Heavily exudative wounds require alginates, hydrofiber, or superabsorbent dressings. Necrotic or sloughy wounds are managed with hydrogel for autolytic debridement or enzymatic debriding agents. Granulating wounds progress well with foam, hydrocolloid, or collagen dressings. Infected or critically colonized wounds benefit from silver-containing dressings or cadexomer iodine. Dressing change frequency depends on the dressing type and exudate volume, ranging from daily (gauze) to every 3 to 7 days (foams, hydrocolloids).

Infection Management

Critical colonization, characterized by delayed healing, friable granulation tissue, increased exudate, and biofilm, should be treated with topical antimicrobials (silver dressings, cadexomer iodine) for 2 to 4 weeks. Clinical infection is indicated by spreading erythema, warmth, purulence, malodor, increased pain, and systemic signs (fever, leukocytosis). Wound cultures should use the Levine technique (rotating the swab over 1 cm-squared of clean wound bed with moderate pressure) rather than superficial swabbing. Systemic antibiotics are indicated only for cellulitis, bacteremia, sepsis, or osteomyelitis and not for local wound infection alone. Osteomyelitis should be suspected in non-healing stage 4 pressure injuries over bony prominences; the "probe to bone" test (positive when a sterile probe contacts bone through the wound) has a specificity of 89 percent. Confirmation is obtained with MRI (sensitivity 90 percent) or bone biopsy (gold standard).

Advanced Therapies (for Non-Healing Wounds)

Negative pressure wound therapy (NPWT/VAC) uses continuous or intermittent suction to promote granulation tissue formation and remove exudate, applied to stage 3 and 4 wounds after debridement (contraindicated in malignancy, untreated osteomyelitis, or when exposed vessels are present). Skin substitutes and cellular tissue products provide bioengineered matrices for chronic non-healing wounds. Hyperbaric oxygen has limited evidence for pressure injuries specifically but may be considered in refractory cases. Surgical reconstruction with flap procedures is reserved for stage 3 and 4 wounds in patients who are surgical candidates, with the critical caveat that the underlying pressure problem must be addressed or recurrence rates of 30 to 60 percent are expected.

Key Clinical Pearls

• Prevention is far more effective and cost-efficient than treatment — every pressure injury should prompt a root cause analysis of prevention failures
• The Braden Scale should be assessed on admission and regularly thereafter; a score ≤18 triggers preventive interventions
• Repositioning every 2 hours and appropriate support surfaces are the foundation of prevention — they are more effective than any treatment once injury occurs
• Stable dry eschar on the heel is the ONE exception to the debridement rule — leave it intact unless infection develops
• Probe-to-bone test is highly specific (89%) for osteomyelitis in non-healing pressure injuries — if positive, obtain MRI and consider bone biopsy
• Malnutrition directly impairs wound healing — pressure injury patients need 30-35 kcal/kg/day and 1.25-1.5 g/kg/day protein
• Deep tissue pressure injuries can evolve rapidly to full-thickness wounds despite optimal care — this does not necessarily represent a care failure; document progression and continued interventions

References

1. 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.
2. Mervis JS, Phillips TJ. Pressure ulcers: pathophysiology, epidemiology, risk factors, and presentation. J Am Acad Dermatol. 2019;81(4):881-890.
3. Qaseem A, Mir TP, Starkey M, Denberg TD. Risk assessment and prevention of pressure ulcers: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2015;162(5):359-369.
4. Langer G, Fink A. Nutritional interventions for preventing and treating pressure ulcers. Cochrane Database Syst Rev. 2014;(6):CD003216.
5. Berlowitz D. Clinical staging and management of pressure-induced skin and soft tissue injury. UpToDate. 2024.

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