Pressure-ulcer staging and prevention

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

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.

Prevention is a care process, not a mattress purchase. Explain risk and movement choices, document who repositions and how heels and devices are offloaded, reduce friction during transfers and manage incontinence without leaving skin wet or occluded. A support surface complements rather than replaces repositioning. Once ulceration occurs, set healing or comfort goals, assess perfusion and nutrition, select moisture-balanced dressings, debride only when appropriate and review the plan whenever the wound or the patient's condition changes.

Key points

Pressure injury is local skin and soft-tissue damage caused by sustained pressure or pressure with shear, usually over bone or beneath a medical device.
Category 1 is intact skin with persistent non-blanching change; in dark skin, new temperature, firmness, bogginess, pain or a purple-grey hue may precede an obvious colour contrast.
Category 2 is partial-thickness skin loss with exposed dermis or an intact or ruptured serum blister; slough, fat and granulation are not category-2 features.
Category 3 exposes full-thickness skin and visible adipose or granulation without exposed fascia, muscle, tendon or bone; undermining and tunnelling may be present.
Category 4 has exposed or directly palpable deep structures such as fascia, muscle, tendon, cartilage or bone and carries high osteomyelitis risk.
If slough or eschar obscures the base, record unstageable until depth is revealed; persistent deep red, maroon or purple discoloration or a blood-filled blister indicates deep-tissue pressure injury.
First-line prevention combines prompt risk and skin assessment, individual repositioning, heel offloading, pressure-redistributing support, moisture control, nutrition and device checks.
NICE adult minimums are repositioning at least every six hours when at risk and every four hours when high risk, but discomfort, tissue response and instability can require a shorter tailored interval.
Do not massage or rub threatened skin, use water-filled gloves or improvised rings, or substitute a risk score for direct inspection.
Systemic antibiotics do not heal an uninfected pressure ulcer; use them for sepsis, spreading cellulitis or osteomyelitis and combine with source, perfusion and wound management.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Sustained tissue pressure

External load between bone and a bed, chair, footwear or device compresses microvessels and deforms cells until local repair can no longer compensate.

Shear and friction

Sliding down a bed stretches deep vessels while the surface stays fixed, and repeated rubbing removes epidermis and lowers tolerance to pressure.

Reduced tissue tolerance

Poor perfusion, neuropathy, oedema, malnutrition, dehydration, fever, ageing and critical illness shorten the pressure exposure that tissue can survive.

Moisture and device load

Urine, stool, sweat and wound fluid macerate barrier, while rigid masks, tubes, casts and splints concentrate pressure in an exact shape.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Microcirculation collapses
Compression obstructs capillary and lymphatic flow, depriving cells of oxygen and preventing removal of metabolites and interstitial fluid.
2
Cells deform directly
High local stress distorts muscle and fat cells near bone and can cause rapid deep injury before conventional ischaemic time has elapsed.
3
Reperfusion amplifies injury
Intermittent pressure release restores oxygen but can generate inflammatory oxidative damage in tissue already compromised by repeated loading.
4
Necrosis tracks outward
Deep muscle and fat damage may extend towards skin, creating delayed discoloration, blistering and an ulcer whose visible opening understates its cavity.
5
Barrier loss permits infection
Once skin opens, colonising organisms access devitalised tissue and can progress to cellulitis, abscess, osteomyelitis and systemic infection.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Category 1 intact injury

Persistent non-blanching local colour, warmth or coolness, firmness, bogginess or pain affects intact skin over a pressure point or device site.

Category 2 partial thickness

A shallow open defect exposes viable pink or red dermis, or a serum blister, without adipose, slough, granulation or deeper tissue.

Category 3 full thickness

The entire skin thickness is lost and adipose or granulation is visible, with possible undermining but no exposed deep fascia, muscle, tendon or bone.

Category 4 deep exposureRed flag

Full-thickness skin and tissue loss exposes or permits direct palpation of fascia, muscle, tendon, cartilage or bone and may tunnel extensively.

Unstageable depth

Slough or eschar covers enough of the base to prevent seeing the deepest tissue, so assigning category 3 or 4 would be guesswork.

Deep-tissue pressure injuryRed flag

Intact or broken skin shows persistent deep red, maroon, purple or dark discoloration or a blood-filled blister after intense pressure or shear.

Device-shaped injury

Damage mirrors tubing, mask, splint, cast or fixation hardware and demands immediate fit and padding review without compromising essential treatment.

Red flags requiring action

Fever, hypotension, spreading erythema, crepitus, foul wet necrosis with decline, pain out of proportion, exposed bone, new neurological deficit, absent pulses, rapidly worsening device indentation or failure to improve after pressure removal requires urgent escalation.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Validated risk and mobility assessmentFirst step
Why
Identify pressure exposure and modifiable tissue vulnerability at admission and after clinical change.
Interpretation and limitations
A tool supports but never replaces clinical judgement; cognition, sensation, mobility, perfusion, nutrition, moisture, devices and previous ulcers all alter actual risk.
02
Head-to-toe skin examination
Why
Detect pre-ulcer change and establish a category using touch as well as sight.
Interpretation and limitations
Inspect and palpate all pressure and device sites with consent, comparing colour, blanching, heat, firmness, moisture and pain; document the deepest directly visible tissue.
03
Wound measurement
Why
Create a reproducible baseline for healing, deterioration and treatment review.
Interpretation and limitations
Record site, category, length, width, depth, undermining, tunnelling, tissue, exudate, edge, surrounding skin and pain; photographs require consent and scale.
04
Perfusion assessment
Why
Identify arterial impairment before heel debridement, compression or reconstructive planning.
Interpretation and limitations
Check pulses, refill, temperature and Doppler pressures or toe tests where relevant; stable dry heel eschar with poor perfusion may be protective and should not be removed reflexively.
05
Nutrition and systemic review
Why
Find intake, weight, swallowing, catabolic disease and deficiencies that limit tissue tolerance and repair.
Interpretation and limitations
Use weight trajectory and dietetic assessment rather than albumin alone, which falls with inflammation; correct deficiencies without promising supplements will overcome ongoing pressure.
06
Infection and osteomyelitis assessment
Why
Distinguish colonisation from cellulitis, deep infection and bone involvement.
Interpretation and limitations
Spreading erythema, heat, swelling, increasing pain, purulence or systemic illness drives cultures and treatment; exposed or probe-accessible bone, deep duration and non-healing lower the imaging and biopsy threshold.
07
Equipment and device audit
Why
Find continuing pressure from beds, chairs, footwear, masks, tubing, splints and transfer technique.
Interpretation and limitations
Map injury shape and loading time and observe care in practice; a prescribed support surface provides no benefit if incorrectly set, bottomed out or bypassed by a device.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Moisture-associated dermatitis

Diffuse irregular superficial erythema and erosion across urine or stool exposure lacks a focal bony-pressure geometry, though both injuries may coexist.

Arterial or diabetic ulcer

Distal ischaemic defects or plantar callus craters require pulse, Doppler and sensory assessment because pressure categories do not replace vascular or foot classification.

Skin tear or friction injury

A trauma-related flap or linear superficial loss follows handling rather than sustained pressure and uses a separate wound classification.

Calciphylaxis or vasculopathy

Severe pain, retiform purple change and necrosis in renal or thrombotic disease reflects vessel occlusion and demands urgent mechanism-specific care.

Inflammatory or malignant ulcer

Pathergic undermining, purpura, induration, everted growth or unexpected bleeding requires dermatology and biopsy rather than repeated pressure staging.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-line prevention sequenceAssess, offload and assign ownershipFirst stepFirst lineA person enters hospital or care with reduced mobility, sensation, perfusion, nutrition or a pressure-causing device.

1Complete risk and skin assessment promptly and after every material change, involving the person and carers in pain, movement and skin-history information.
2Place high-risk adults on an appropriate high-specification foam or higher-level pressure-redistributing surface, float heels and pad or reposition devices without compromising function.
3Write a repositioning and inspection schedule with technique, assistance and named responsibility and review tissue response rather than relying on a turn chart alone.

02Adult repositioning minimumIndividualise beyond the clockAn adult is assessed at risk or high risk and can be repositioned safely.

1Encourage or assist a position change at least every six hours for at-risk adults and at least every four hours for high-risk adults, following current NICE minimums.
2Shorten the interval when pain, persistent discoloration, device load, poor perfusion or surface failure indicates inadequate unloading and adapt movement for respiratory or spinal precautions.
3AlternativeRecord position, skin response, comfort and refusals and solve barriers collaboratively rather than documenting non-compliance without an alternative.

03First-line ulcer careRemove cause and create a healing environmentFirst lineA pressure injury is confirmed and no emergency infection or ischaemia requires immediate transfer.

1Offload the site completely where feasible, upgrade the mattress or seat surface, control shear during transfers and protect skin from urine, stool, sweat and adhesive trauma.
2Clean with an appropriate solution, select a moisture-balancing dressing based on exudate, pain and surrounding skin and give analgesia before handling.
3EscalationSet nutrition, mobility and continence plans and review category and dimensions regularly, escalating if deeper tissue declares itself despite correct unloading.

04Debridement decisionRemove devitalised tissue only when it helpsSlough or eschar obscures a wound or supports infection, odour or delayed healing.

1Assess vascular supply, bleeding risk, pain, goals and whether stable dry heel eschar is protecting an ischaemic surface before selecting any method.
2Use autolytic debridement first when clinically appropriate, or trained sharp debridement when speed is necessary and perfusion and analgesia are adequate.
3Do not use routine debridement to force a stage label; treat spreading infection surgically when required and document the category once actual depth becomes visible.

05Infection escalationTreat tissue invasion rather than surface floraEscalationSpreading cellulitis, sepsis, wet necrosis or suspected osteomyelitis develops.

1Obtain appropriate deep specimens and blood cultures when feasible without delaying treatment and begin systemic antibiotics through local severe-skin or bone-infection guidance.
2Arrange urgent surgical, tissue-viability and vascular assessment for drainage, necrosis, exposed bone or impaired perfusion and continue complete pressure relief.
3Review antibiotic response and source control frequently and stop treating colonisation once clinical infection has resolved.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Deep tissue destruction

Progression can expose muscle, tendon, joint and bone, cause contracture and require prolonged reconstruction or comfort-focused wound care.

Cellulitis and sepsis

Devitalised tissue supports invasive bacteria, leading to spreading infection, bacteraemia, shock and death in physiologically vulnerable patients.

Osteomyelitis

Chronic deep ulcers over sacrum, heel or other bone can seed cortex and marrow, complicating closure and requiring prolonged combined treatment.

Pain and functional decline

Wound, dressing and reposition pain disrupts sleep and movement, which can worsen immobility, nutrition, delirium, mood and future pressure exposure.

Recurrence and care harm

Scarred tissue fails under lower load, while poor handover, incorrect equipment or inequitable skin assessment can reproduce preventable injury after transfer.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Inspect high-risk skin and every device contact at the frequency set by risk and after transfer, surgery, deterioration, diarrhoea, sedation or equipment change.
Record category, dimensions, undermining, tissue, exudate, surrounding skin and pain consistently, noting when deep injury evolves despite an initially intact surface.
Audit whether repositioning, heel suspension and device relief actually occurred and whether the patient could tolerate them, then address staffing, pain or equipment barriers.
Review weight, intake, swallowing, hydration and dietetic plan and investigate unintentional loss rather than using albumin as a stand-alone nutrition score.
Monitor for spreading redness, warmth, swelling, increased pain, purulence, fever, delirium and bone exposure and activate the infection pathway promptly.
Before discharge or transfer, communicate every injury and prevention plan, support-surface need, dressing, reposition interval and responsible follow-up service.
After closure, continue offloading and risk review because scar has reduced tensile strength and recurrence is common at the same pressure point.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Muscle can fail first

Deep tissue near bone may be injured before surface breakdown, explaining a painful purple intact area that later opens despite immediate correct offloading.

Stage describes depth only

A higher category does not quantify infection, pain, prognosis or preventability, and a healing category-4 ulcer never reverses to category 3.

Dark skin needs touch

Temperature, firmness, bogginess and pain may identify category-1 injury earlier than visible non-blanching redness in richly pigmented skin.

Slough hides rather than upgrades

An obscured base is unstageable, not automatically category 4; the true depth is recorded only when visible or directly palpable.

Device function still matters

Relieving mask or tube pressure must be balanced with oxygenation, immobilisation or drainage needs through redesign and frequent checks, not unsafe removal.

A mattress cannot turn

Pressure redistribution reduces peak load but cannot replace movement, heel suspension, device review and moisture management in a high-risk person.

11Common pitfallsFrequent interpretation and management errors.

01
Searching only for red colour and missing purple-grey, temperature, firmness or pain changes in darker skin.
02
Calling moisture-associated dermatitis category 2 despite diffuse superficial inflammation outside a pressure pattern.
03
Assigning category 3 or 4 through an eschar-covered base that has not been visualised.
04
Massaging non-blanching skin or using improvised ring devices that concentrate pressure at their edges.
05
Relying on a mattress order while repositioning, heels, devices and transfer shear remain unaddressed.
06
Giving systemic antibiotic to make an uninfected colonised ulcer heal faster.
07
Removing stable dry heel eschar before assessing ischaemia and the purpose of its protective cover.
08
Documenting refusal without treating pain, explaining choices or offering a tolerable alternative position.