Pressure Injuries

The mechanism is hydraulic. Arterial capillaries fill at roughly 32 mm Hg; venous capillaries close at 8–12 mm Hg. External pressure above the arterial filling pressure stops blood from flowing in, and pressure above the venous closing pressure stops it from draining out. The result is microvascular occlusion: the compressed tissue becomes ischemic and hypoxic, toxic metabolites accumulate, the cells acidify, and they die by apoptosis. A hospital mattress pressing a sacrum against a bed frame can exceed these numbers for hours at a time.

The time factor is shorter than most students expect: as little as 2 hours of immobility in a bedridden patient — or a patient on an operating table — is sufficient to lay the foundation of an injury. That number is the origin of the every-2-hours turn schedule. The classic locations are wherever bone sits close to skin: the sacrum, ischial tuberosities, and greater trochanters account for about 70% of pressure injuries, with the occiput, scapula, elbow, heel, lateral malleolus, shoulder, and ear making up most of the rest. Rigid medical devices — endotracheal tubes, cervical collars, nasal cannulas, casts — create the same injury at sites far from any bony prominence, so the skin under every device is part of the inspection.

Pure vertical pressure rarely acts alone. Shear happens when tissue layers slide over each other — the classic example is a patient sliding down in a raised bed: the skin sticks to the sheets while the skeleton slides, so blood vessels between the layers stretch and break. Shear injures deep tissue while the surface can still look intact, which is why head-of-bed elevation is capped in the prevention bundle. Friction — skin rubbing across a surface when a patient is dragged rather than lifted — generates heat and strips the superficial skin layers, compounding the damage.

The third accomplice is moisture. Skin exposed to sweat, urine, or water for extended periods becomes soggy, wrinkly, and whiter than usual — maceration — and macerated skin breaks down far more easily under the same pressure. Prolonged urine or stool exposure can also injure skin on its own as incontinence-associated dermatitis (IAD) — an irritant contact dermatitis that is a different condition from a pressure injury (top-down chemical and moisture damage rather than bottom-up ischemia) and must be distinguished from one at the bedside.

Staging belongs to the National Pressure Injury Advisory Panel (NPIAP, formerly NPUAP), whose 2016 system is the current framework. That revision also renamed the condition: “pressure ulcer” became “pressure injury” because an ulcer cannot describe Stage 1 or deep tissue pressure injury, where the skin is still intact — “an ulcer cannot be present without an injury, but an injury can be present without an ulcer.” Tissue damage begins histologically before anything is visible on the surface.

The stages are a ladder of anatomic depth: Stage 1 is intact skin with non-blanchable erythema; Stage 2 is partial-thickness skin loss with exposed dermis; Stage 3 is full-thickness loss with visible fat; Stage 4 reaches bone, tendon, ligament, cartilage, or muscle. Two categories sit beside the ladder rather than on it. Unstageable means full-thickness loss whose true depth cannot be confirmed because slough or eschar hides the wound base. Deep tissue pressure injury (DTPI) is persistent non-blanchable deep red, maroon, or purple discoloration — the bruise-like signature of severe damage rising from below, distinct from Stage 1’s red erythema. Device-related injuries use the same ladder; injuries of mucosal membranes cannot be staged with the skin system at all.

One staging-adjacent rule saves limbs: stable, dry, adherent eschar on a heel or an ischemic limb is not typically removed. That intact black cap is serving as a biological cover over tissue with too little blood supply to heal an open wound.

The epidemiology explains the intensity of the prevention culture: up to 3 million US adults are affected annually, prevalence runs 10–18% in acute care and over 25% in critically ill patients, and hospital-acquired pressure injuries cost more than $26.8 billion a year. Once an injury exists, healing is slow and uncertain — only about half of pressure injuries heal within 12 months, and the deeper the stage, the worse the odds. Older patients with a pressure injury carry a 3.6-fold higher mortality within 21 months. Prevention is therefore the most important management strategy — not a platitude but the literal treatment plan.

Prevention starts with knowing who is at risk, and the standard instrument is the Braden Scale: six subscales — sensory perception, moisture, activity, mobility, nutrition, and friction/shear — each scored 1–4 (friction/shear 1–3), totaling 6–23 with lower meaning higher risk. A total of ≤ 18 marks the onset of risk, and the bands below it grade intensity. The score is not a label; it is a work order — each deficient subscale maps to its own set of interventions, so a patient failing on moisture gets barrier care while a patient failing on mobility gets the turn schedule and support surface.