Detect pressure injury early across skin tones, assign a defensible category without understaging concealed depth, remove pressure and shear, and deliver individualised prevention, wound, nutrition and infection care.
Pressure injury reflects the interaction between tissue load and tissue tolerance. Immobility, reduced sensation, poor perfusion, oedema, malnutrition, moisture and medical devices lower the duration or intensity of pressure that skin and deeper tissues can withstand. Damage may begin in muscle over a bony prominence before the epidermis breaks, explaining why a purple intact heel can deteriorate after offloading and why surface dimensions can underestimate depth. Common sites include sacrum, heels, trochanters, ischia, occiput and areas beneath oxygen tubing, casts, splints and catheters.
Assess in the person's usual pigmentation. Non-blanching erythema may be difficult to see in brown or black skin and can present as a new violet, blue, grey, brown or unusually dark area. Compare temperature, firmness and moisture with adjacent or contralateral tissue and ask about pain, burning or numbness. Do not stage mucosal pressure injury because keratinised layers are absent, and identify device-related injuries by their pattern while using the same category system on skin.
External load between bone and a bed, chair, footwear or device compresses microvessels and deforms cells until local repair can no longer compensate.
Sliding down a bed stretches deep vessels while the surface stays fixed, and repeated rubbing removes epidermis and lowers tolerance to pressure.
Poor perfusion, neuropathy, oedema, malnutrition, dehydration, fever, ageing and critical illness shorten the pressure exposure that tissue can survive.
Urine, stool, sweat and wound fluid macerate barrier, while rigid masks, tubes, casts and splints concentrate pressure in an exact shape.
Compression obstructs capillary and lymphatic flow, depriving cells of oxygen and preventing removal of metabolites and interstitial fluid.
High local stress distorts muscle and fat cells near bone and can cause rapid deep injury before conventional ischaemic time has elapsed.
Intermittent pressure release restores oxygen but can generate inflammatory oxidative damage in tissue already compromised by repeated loading.
Deep muscle and fat damage may extend towards skin, creating delayed discoloration, blistering and an ulcer whose visible opening understates its cavity.
Once skin opens, colonising organisms access devitalised tissue and can progress to cellulitis, abscess, osteomyelitis and systemic infection.
Persistent non-blanching local colour, warmth or coolness, firmness, bogginess or pain affects intact skin over a pressure point or device site.
A shallow open defect exposes viable pink or red dermis, or a serum blister, without adipose, slough, granulation or deeper tissue.
The entire skin thickness is lost and adipose or granulation is visible, with possible undermining but no exposed deep fascia, muscle, tendon or bone.
Full-thickness skin and tissue loss exposes or permits direct palpation of fascia, muscle, tendon, cartilage or bone and may tunnel extensively.
Slough or eschar covers enough of the base to prevent seeing the deepest tissue, so assigning category 3 or 4 would be guesswork.
Intact or broken skin shows persistent deep red, maroon, purple or dark discoloration or a blood-filled blister after intense pressure or shear.
Damage mirrors tubing, mask, splint, cast or fixation hardware and demands immediate fit and padding review without compromising essential treatment.
Diffuse irregular superficial erythema and erosion across urine or stool exposure lacks a focal bony-pressure geometry, though both injuries may coexist.
Distal ischaemic defects or plantar callus craters require pulse, Doppler and sensory assessment because pressure categories do not replace vascular or foot classification.
A trauma-related flap or linear superficial loss follows handling rather than sustained pressure and uses a separate wound classification.
Severe pain, retiform purple change and necrosis in renal or thrombotic disease reflects vessel occlusion and demands urgent mechanism-specific care.
Pathergic undermining, purpura, induration, everted growth or unexpected bleeding requires dermatology and biopsy rather than repeated pressure staging.
Progression can expose muscle, tendon, joint and bone, cause contracture and require prolonged reconstruction or comfort-focused wound care.
Devitalised tissue supports invasive bacteria, leading to spreading infection, bacteraemia, shock and death in physiologically vulnerable patients.
Chronic deep ulcers over sacrum, heel or other bone can seed cortex and marrow, complicating closure and requiring prolonged combined treatment.
Wound, dressing and reposition pain disrupts sleep and movement, which can worsen immobility, nutrition, delirium, mood and future pressure exposure.
Scarred tissue fails under lower load, while poor handover, incorrect equipment or inequitable skin assessment can reproduce preventable injury after transfer.
Deep tissue near bone may be injured before surface breakdown, explaining a painful purple intact area that later opens despite immediate correct offloading.
A higher category does not quantify infection, pain, prognosis or preventability, and a healing category-4 ulcer never reverses to category 3.
Temperature, firmness, bogginess and pain may identify category-1 injury earlier than visible non-blanching redness in richly pigmented skin.
An obscured base is unstageable, not automatically category 4; the true depth is recorded only when visible or directly palpable.
Relieving mask or tube pressure must be balanced with oxygenation, immobilisation or drainage needs through redesign and frequent checks, not unsafe removal.
Pressure redistribution reduces peak load but cannot replace movement, heel suspension, device review and moisture management in a high-risk person.
Searching only for red colour and missing purple-grey, temperature, firmness or pain changes in darker skin.
Calling moisture-associated dermatitis category 2 despite diffuse superficial inflammation outside a pressure pattern.
Assigning category 3 or 4 through an eschar-covered base that has not been visualised.
Massaging non-blanching skin or using improvised ring devices that concentrate pressure at their edges.
Relying on a mattress order while repositioning, heels, devices and transfer shear remain unaddressed.
Giving systemic antibiotic to make an uninfected colonised ulcer heal faster.
Removing stable dry heel eschar before assessing ischaemia and the purpose of its protective cover.
Documenting refusal without treating pain, explaining choices or offering a tolerable alternative position.
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An immobile patient develops a persistently painful maroon-purple heel with intact skin, local bogginess and a blood-filled blister after prolonged pressure. Which classification is most appropriate?
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
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