What is a pressure injury and who is most at risk?

A pressure injury — also called a pressure ulcer, pressure sore, or bedsore — is localised damage to skin and underlying soft tissue caused by sustained pressure, usually over a bony prominence such as the sacrum, heels, or hips. The pressure cuts off the blood supply, causing tissue death. Anyone who cannot reposition themselves is at risk: people who are bed-bound, chair-bound, sedated, or paralysed. Other major risk factors include incontinence and moisture, malnutrition, diabetes, poor circulation, and very old or very thin skin. About 20–30% of aged-care residents and 10–15% of hospital inpatients have a pressure injury at any time.

How are pressure injuries staged?

Pressure injuries are staged by how deep the tissue damage is. Stage 1 is non-blanchable redness on intact skin — apply pressure and the redness does not go white. In darker skin tones this can appear as a purple or blue patch, firmness, or temperature change. Stage 2 is a shallow open wound with a pink-red moist wound bed, or an intact blister filled with fluid. Stage 3 is full-thickness skin loss exposing fat but not deeper structures. Stage 4 is the most severe, with bone, tendon, or muscle exposed — carrying a high risk of bone infection. Unstageable means the wound base is covered by dead tissue, so the true depth cannot be assessed until it is cleaned.

What is deep tissue injury and why is it serious?

Deep tissue injury (DTI) is a particularly deceptive type of pressure injury. It looks like persistent dark purple or maroon discolouration of intact skin, but this surface appearance hides deep damage that has already occurred at the bone-muscle interface. The overlying skin looks relatively unharmed, but the tissue below has been destroyed by the pressure and shearing forces acting at that interface. Within hours to days, even with optimal care, a DTI can evolve into a Stage 3 or Stage 4 wound as the damage declares itself outward through the skin. Families and care staff need to understand that this progression is not a failure of care — it is the nature of the injury.

What is the SSKIN bundle for preventing pressure injuries?

SSKIN is a mnemonic for the five key components of pressure injury prevention. S is Support surface — a pressure-redistributing mattress (static foam or dynamic alternating-air) and an appropriate cushion for anyone spending significant time sitting. S is Skin assessment — a head-to-heel inspection at admission and at least daily in high-risk settings. K is Keep moving — repositioning every two hours in bed and every hour in a chair, with heels kept floating off the mattress. I is Incontinence and moisture management — prompt clothing and linen changes, pH-balanced skin cleansers, and barrier creams. N is Nutrition — adequate protein (1.2–1.5 g/kg/day), calories, fluids, and micronutrients to support tissue repair.

When should I be worried about infection in a pressure wound?

Chronic wounds are always colonised by bacteria — that alone does not mean the wound is infected and does not warrant antibiotic treatment. Treat for infection only when there are clear clinical signs: increasing redness spreading around the wound edge, increasing or changing exudate (particularly if it becomes cloudy or smells offensive), fluctuance (fluid under the skin), increasing wound pain, or systemic signs such as fever, raised heart rate, confusion in an older person, or elevated inflammatory markers on blood tests. Swabbing is useful only when infection is already clinically diagnosed — routine swabbing of every chronic wound is strongly discouraged and drives unnecessary antibiotic use.

What dressing should be used on a pressure injury?

Dressing choice depends primarily on the stage and how much fluid the wound is producing. Stage 1 injuries need pressure offloading above all — a transparent film or thin foam dressing protects the skin but the offloading is the treatment. Stage 2 wounds with low exudate suit hydrocolloid dressings (DuoDerm, Comfeel) changed every 3–7 days; moderate exudate suits foam dressings (Allevyn, Mepilex). Stage 3–4 wounds need cavity filling with alginate (Kaltostat) or hydrofibre (Aquacel) for high exudate, covered by foam. Silver dressings are not used routinely — they are reserved for wounds with confirmed local infection, for a limited two-to-four-week period.

Pressure injury (pressure ulcer)

Pressure injuries: staging, prevention, and wound management

By Dr HB Lo, FACRRM Reviewed 24 October 2026 11 min read

Pressure injuries form when sustained pressure over a bony prominence — sacrum, heels, hips — cuts off blood supply and causes tissue death. They range from non-blanchable skin redness (Stage 1) through partial and full-thickness skin loss (Stages 2–4) to bone-exposing wounds with osteomyelitis risk.

Prevention rests on the SSKIN bundle: appropriate support surface, regular skin inspection, repositioning every two hours, incontinence and moisture management, and adequate protein intake. Treatment follows the TIME framework — tissue debridement, infection control, moisture balance, and edge advancement — with dressing choice matched to wound stage and exudate.

Pressure injuries — also called pressure ulcers, pressure sores, or bedsores — affect approximately 20–30% of aged-care facility residents, 10–15% of acute hospital inpatients, and around 5% of people receiving community-based home care in Australia. The annual cost to the Australian health system is estimated at A$9.1 billion according to the Australian Commission on Safety and Quality in Health Care (ACSQHC). Hospital-acquired pressure injuries are a notifiable indicator under the National Aged Care Mandatory Quality Indicator Program.

Beyond the economic cost, pressure injuries cause significant pain, prolong hospital admissions by four to ten additional days for Stage 3 and Stage 4 injuries, increase infection risk, and substantially worsen quality of life. In frail older adults, Stage 4 sacral pressure injuries carry a one-year mortality rate of up to 60–70%. Understanding prevention and early-stage management in general practice substantially reduces the burden of advanced disease.

A. Core clinical — the AU general-practice framework

Pathophysiology

Four mechanical forces combine to cause pressure injuries. Pressure is the primary driver: tissue capillary perfusion is impaired at pressures above approximately 32 mmHg sustained for a prolonged period. Shear — the sliding movement of bone against deep tissue during repositioning or sliding down a bed — generates the highest stress at the bone-muscle interface, explaining why deep tissue injury appears superficial while being deeply destructive. Friction abrades the skin surface, compromising its barrier function. Microclimate — skin temperature and moisture from incontinence or sweat — softens and weakens the epidermis, reducing the pressure required to cause injury.

A key clinical insight is that deep tissue injury (DTI) originates at the bone-muscle interface and propagates outward. By the time discolouration becomes visible at the skin surface, significant deep tissue destruction has already occurred. This is why what appears to be a minor Stage 1 presentation can deteriorate to Stage 3 or Stage 4 within hours to days even under optimal care.

Risk assessment

The NPIAP / EPUAP / PPPIA 2019 International Guideline and Wounds Australia 2024 standards recommend formal risk assessment on admission to hospital or aged care, at 24 hours, and with any change in clinical condition. The Braden Scale (scores ≤18 indicate at-risk; lower scores indicate higher risk) and the Waterlow Scale are the most widely used validated tools in Australian practice.

Risk factors to document systematically include:

Mobility: bed-bound, chair-bound, paralysis, sedation, immobilisation in plaster or splint, prolonged surgery over two hours
Sensation: spinal cord injury, peripheral neuropathy, cognitive impairment or altered consciousness
Moisture: urinary or faecal incontinence, wound exudate, perspiration
Nutrition: malnutrition (Malnutrition Universal Screening Tool score), albumin below 30 g/L, significant unintentional weight loss, BMI below 20
Perfusion: hypotension, peripheral vascular disease, anaemia, smoking history
Comorbidities: diabetes, chronic kidney disease, oedema, immunosuppression
Previous pressure injury: the single strongest predictor of recurrence

Staging

The NPIAP 2016 classification, adopted by Wounds Australia and the ACSQHC Clinical Care Standard (2022), defines the following categories:

Stage 1: Non-blanchable erythema of intact skin. In dark skin tones, Stage 1 may present as persistent discolouration, warmth, firmness, or oedema rather than visible erythema — active palpation and temperature assessment are essential.

Stage 2: Partial-thickness skin loss exposing the dermis. Wound bed is pink or red and moist; may present as an intact or ruptured serum-filled blister. Importantly, Stage 2 should not be applied to moisture-associated skin damage (incontinence-associated dermatitis), skin tears, or medical-adhesive injuries — these are distinct entities requiring different management.

Stage 3: Full-thickness skin loss exposing subcutaneous fat. May show granulation tissue, slough, undermining, or tunnelling. Depth varies by anatomical site — shallow over the nasal bridge, occiput, or malleolus where fat is minimal.

Stage 4: Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone. Osteomyelitis risk is high; bone biopsy and targeted antibiotic therapy may be required.

Unstageable: Full-thickness loss obscured by slough or eschar; the actual depth cannot be determined until debridement. The exception is stable dry eschar on the heel of an ischaemic limb — this should not be debrided, as it provides natural biological cover.

Deep Tissue Injury (DTI): Persistent non-blanchable dark red, maroon, or purple discolouration of intact or non-intact skin, or a blood-filled blister, indicating deep damage at the bone-muscle interface that may evolve rapidly to Stage 3–4.

Medical-Device-Related Pressure Injury (MDRPI): Caused by a device used for diagnosis or treatment — the injury follows the shape of the device (nasogastric tube at the nares, CPAP mask at the nasal bridge, endotracheal tube at the lip). Staged using the standard NPIAP system.

Prevention — the SSKIN bundle

Per the NPIAP / EPUAP / PPPIA 2019 guideline, Wounds Australia standards, and eTG, prevention centres on the SSKIN bundle:

Surface: A pressure-redistributing mattress — static high-specification foam or dynamic alternating-air/low-air-loss — for all at-risk patients. A 2018 Cochrane review by McInnes and colleagues confirmed alternating-air mattresses reduce pressure injury incidence compared with standard hospital foam. A pressure-redistributing cushion is required for anyone seated for four or more hours daily.

Skin assessment: Head-to-heel inspection at admission, every 24 hours (or each shift in acute care), and with any clinical change. Always lift the heel to inspect it — heel pressure injuries are the most frequently missed. Document with photographs and a body map.

Keep moving: Individualised repositioning schedule — the standard defaults are two-hourly in bed and hourly in a chair, with heels kept floating. The 30-degree tilt is preferred over the full 90-degree lateral position as it reduces trochanteric pressure.

Incontinence and moisture: Prompt clothing and linen changes after incontinence, pH-balanced skin cleanser (not soap), barrier cream or film product, and active management of the underlying continence problem.

Nutrition: Protein 1.2–1.5 g/kg/day, energy 30 kcal/kg/day, fluid 30 mL/kg/day, adequate micronutrients. Refer to an accredited practising dietitian via the GP Chronic Condition Management Plan for patients with Stage 2–4 injuries or confirmed malnutrition.

B. Wound staging evidence and treatment

Treatment by stage

Stage 1: Offloading is the definitive intervention. A transparent film or thin foam dressing protects the skin from friction, but the dressing does not treat the injury — removing the pressure does. Reassess in 24–48 hours; failure to resolve indicates inadequate pressure relief, not an inadequate dressing.

Stage 2: Cleanse with normal saline (avoid antiseptics — they damage granulation tissue). Hydrocolloid dressings (DuoDerm, Comfeel) for low exudate; foam dressings (Allevyn, Mepilex) for moderate exudate. Change every three to seven days or when strikethrough is visible.

Stage 3: Cleanse with normal saline. Fill cavities with alginate (Kaltostat) or hydrofibre (Aquacel) for high exudate; cover with foam. Consider negative pressure wound therapy for large, exudating, granulating wounds. Change every one to three days. Multidisciplinary involvement begins here — wound clinical nurse consultant, dietitian, occupational therapist for equipment.

Stage 4: As Stage 3, with mandatory multidisciplinary involvement including plastic surgery review for flap reconstruction in appropriate patients, infectious diseases for osteomyelitis management, and specialist wound nursing. MRI (item 63551) and bone biopsy direct antibiotic therapy in suspected osteomyelitis.

Unstageable: Debridement is required to stage and treat the wound unless stable dry eschar on an ischaemic limb. Autolytic debridement (hydrogel under an occlusive dressing) is the safest for the general practitioner context; sharp surgical debridement is faster but requires specialist involvement.

DTI: Offload aggressively. Do not debride intact DTI — it may stabilise. Reassess daily and counsel the patient and family that evolution to Stage 3 or 4 is possible despite optimal care.

The TIME framework for chronic wounds

Per eTG wound management guidelines:

T — Tissue: Remove non-viable slough and eschar
I — Infection/inflammation: Treat confirmed local infection (not mere colonisation) with topical antimicrobials; systemic antibiotics for spreading or systemic infection
M — Moisture: Too dry prevents autolysis; too wet causes maceration and peri-wound breakdown
E — Edge: Rolled wound edges (epibole) impede epithelial migration and require debridement

C. Adjunct therapies and evidence

Silver dressings: Vermeulen et al. 2007 Cochrane review found no clear benefit of silver over standard care; NICE NG142 (2019) recommends against routine use. Reserve silver dressings for clinically infected wounds for a limited period of two to four weeks, then switch to standard dressings. Routine silver use risks cytotoxicity to granulation tissue and emerging antimicrobial resistance.

Negative pressure wound therapy (NPWT): Dumville et al. 2015 Cochrane review found modest evidence for accelerated healing in selected Stage 3–4 wounds. Contraindicated in malignant wounds, untreated osteomyelitis, fistulas, and wounds with exposed vessels. Community and home-care NPWT is funded through My Aged Care, DVA, and NDIS where applicable.

Disease-specific oral nutritional supplements: Cereda et al. 2015 (JAMA Intern Med) randomised 200 malnourished patients with Stage 2–4 pressure injuries to disease-specific oral nutritional supplements (including arginine, glutamine, zinc, and vitamin C) versus standard isocaloric supplements, finding superior wound area reduction at eight weeks. This supports referring malnourished patients with Stage 2–4 injuries to a dietitian for disease-specific supplementation.

Pain management: Pressure injury pain is consistently under-recognised. Assess pain at rest, during dressing changes (use the Abbey Pain Scale in non-verbal or dementia patients), and with movement. Topical lidocaine 2% gel or EMLA before debridement; regular paracetamol; opioids (oxycodone or morphine) for dressing changes in advanced wounds. Multimodal non-pharmacological approaches — pre-medication 30 minutes before dressing changes, distraction, gentle positioning — reduce procedure-related pain.

D. Australian operations

Standard GP consultations (MBS items 23, 36, 44) cover wound assessment and management. Practice nurse wound management (item 10997) enables nursing-led dressing changes for and on behalf of a GP for patients with chronic disease and complex care needs. Telehealth consultations with photograph-based wound review (video item 91790) are rebatable for patients with an existing GP relationship and are appropriate for ongoing wound monitoring in community settings.

The GP Chronic Condition Management Plan (items 965 and 967, replacing GPMP/TCA since 1 July 2025) gates allied-health referrals for pressure-injury management — up to five visits per year across dietitian, podiatrist, occupational therapist, and physiotherapist. Case conferencing (items 132, 133) supports multidisciplinary team coordination for complex Stage 3–4 injuries in community settings.

Wound dressing funding: Dressings are not funded on the PBS. Funding pathways vary by setting and eligibility: public hospital or community health programs (state-funded in NSW, Victoria, and other states), DVA Rehabilitation Appliances Program (RAP) for eligible veterans, My Aged Care Home Care Package (Level 2–4) consumables, NDIS for participants where the wound is disability-related, and private out-of-pocket otherwise.

Pressure-redistribution equipment: Mattresses and cushions are funded through NDIS Assistive Technology, My Aged Care Home Care Packages, DVA RAP, or workers’ compensation. Occupational therapist assessment and prescription is required for NDIS and My Aged Care funding. My Aged Care is the entry point for aged-care funding including community nursing and equipment.

Mandatory reporting and medico-legal obligations: Hospital-acquired pressure injuries are a reportable indicator under ACSQHC’s hospital-acquired complications framework. Stage 3 or Stage 4 pressure injuries in RACFs must be reported under the National Aged Care Mandatory Quality Indicator Program. Document risk assessment, prevention measures, and wound management contemporaneously. Coronial considerations arise when pressure injuries contribute to death in care settings.

E. Special populations

Aged care and end-of-life: Pressure injury risk in frail older adults with advanced dementia, terminal illness, or multi-organ failure may be irreducible despite full SSKIN compliance. The Kennedy Terminal Ulcer (KTU) is a recognised variant of skin failure in the dying patient — a pear-shaped or horseshoe sacral lesion appearing within hours to days of death and progressing rapidly regardless of care. When skin failure is the likely diagnosis, the goal of care shifts from healing to comfort: minimise dressing changes, control pain, manage odour with metronidazole gel, and ensure the family understands that this is a feature of the dying process, not a preventable adverse event. This reframing belongs in advance-care-planning conversations.

Spinal cord injury: Lifetime pressure injury risk exceeds 85% in people with spinal cord injury. Annual RACGP health assessments for SCI patients should include pressure injury risk review, equipment adequacy, seating assessment, and skin inspection. This population benefits from specialist SCI rehabilitation input for pressure injury prevention protocols.

Diabetes: Peripheral neuropathy removes protective pain sensation, peripheral vascular disease impairs tissue perfusion and wound healing, and hyperglycaemia impairs neutrophil function. Any pressure injury in a person with diabetes warrants earlier specialist referral and more aggressive multidisciplinary management than the stage alone would suggest. Optimising glycaemic control supports wound healing.

Children: Paediatric pressure injuries are most common in ICU, cardiac surgery, and haematology-oncology settings. Medical-device-related injuries (particularly CPAP masks, cervical collars, and nasogastric tube pressure) are the most frequent cause. Prevention and management principles mirror the adult approach, adjusted for size and developmental stage.

When to escalate

Refer urgently or to an emergency department for:

Sepsis from an infected pressure injury — fever, tachycardia, hypotension, or acute confusion in an older person; activate the sepsis pathway immediately
Rapidly progressive erythema, disproportionate pain, or crepitus at the wound site — possible necrotising soft-tissue infection, a surgical emergency requiring immediate specialist assessment
Exposed bone with constitutional symptoms — osteomyelitis requiring MRI and bone biopsy
Stage 3 or 4 wound not responding to four weeks of optimal wound-bed preparation — refer to wound clinical nurse consultant or specialist wound clinic

Routine referral within one to four weeks is appropriate for Stage 2–3 wounds not progressing, new patients requiring GPCCMP allied-health referral, and OT seating and equipment assessment.

What this article is and is not

This article draws on the NPIAP / EPUAP / PPPIA 2019 International Guideline, Wounds Australia 2024 standards, the ACSQHC Pressure Injury Clinical Care Standard (2022), eTG wound management guidelines, and major wound-care trials. It is general patient information, not personalised medical advice, and does not create a doctor–patient relationship. Specific wound management decisions — including dressing choice, debridement, antibiotic use, and specialist referral timing — are made with your GP, wound nurse, or treating team based on your individual clinical situation.

Australian consumer resources: HealthDirect — Pressure injuries, Better Health Channel — Pressure injury, and My Aged Care for equipment and care funding.

Sources cited

Frequently asked questions

What is a pressure injury and who is most at risk?

A pressure injury — also called a pressure ulcer, pressure sore, or bedsore — is localised damage to skin and underlying soft tissue caused by sustained pressure, usually over a bony prominence such as the sacrum, heels, or hips. The pressure cuts off the blood supply, causing tissue death. Anyone who cannot reposition themselves is at risk: people who are bed-bound, chair-bound, sedated, or paralysed. Other major risk factors include incontinence and moisture, malnutrition, diabetes, poor circulation, and very old or very thin skin. About 20–30% of aged-care residents and 10–15% of hospital inpatients have a pressure injury at any time.
How are pressure injuries staged?

Pressure injuries are staged by how deep the tissue damage is. Stage 1 is non-blanchable redness on intact skin — apply pressure and the redness does not go white. In darker skin tones this can appear as a purple or blue patch, firmness, or temperature change. Stage 2 is a shallow open wound with a pink-red moist wound bed, or an intact blister filled with fluid. Stage 3 is full-thickness skin loss exposing fat but not deeper structures. Stage 4 is the most severe, with bone, tendon, or muscle exposed — carrying a high risk of bone infection. Unstageable means the wound base is covered by dead tissue, so the true depth cannot be assessed until it is cleaned.
What is deep tissue injury and why is it serious?

Deep tissue injury (DTI) is a particularly deceptive type of pressure injury. It looks like persistent dark purple or maroon discolouration of intact skin, but this surface appearance hides deep damage that has already occurred at the bone-muscle interface. The overlying skin looks relatively unharmed, but the tissue below has been destroyed by the pressure and shearing forces acting at that interface. Within hours to days, even with optimal care, a DTI can evolve into a Stage 3 or Stage 4 wound as the damage declares itself outward through the skin. Families and care staff need to understand that this progression is not a failure of care — it is the nature of the injury.
What is the SSKIN bundle for preventing pressure injuries?

SSKIN is a mnemonic for the five key components of pressure injury prevention. S is Support surface — a pressure-redistributing mattress (static foam or dynamic alternating-air) and an appropriate cushion for anyone spending significant time sitting. S is Skin assessment — a head-to-heel inspection at admission and at least daily in high-risk settings. K is Keep moving — repositioning every two hours in bed and every hour in a chair, with heels kept floating off the mattress. I is Incontinence and moisture management — prompt clothing and linen changes, pH-balanced skin cleansers, and barrier creams. N is Nutrition — adequate protein (1.2–1.5 g/kg/day), calories, fluids, and micronutrients to support tissue repair.
When should I be worried about infection in a pressure wound?

Chronic wounds are always colonised by bacteria — that alone does not mean the wound is infected and does not warrant antibiotic treatment. Treat for infection only when there are clear clinical signs: increasing redness spreading around the wound edge, increasing or changing exudate (particularly if it becomes cloudy or smells offensive), fluctuance (fluid under the skin), increasing wound pain, or systemic signs such as fever, raised heart rate, confusion in an older person, or elevated inflammatory markers on blood tests. Swabbing is useful only when infection is already clinically diagnosed — routine swabbing of every chronic wound is strongly discouraged and drives unnecessary antibiotic use.
What dressing should be used on a pressure injury?

Dressing choice depends primarily on the stage and how much fluid the wound is producing. Stage 1 injuries need pressure offloading above all — a transparent film or thin foam dressing protects the skin but the offloading is the treatment. Stage 2 wounds with low exudate suit hydrocolloid dressings (DuoDerm, Comfeel) changed every 3–7 days; moderate exudate suits foam dressings (Allevyn, Mepilex). Stage 3–4 wounds need cavity filling with alginate (Kaltostat) or hydrofibre (Aquacel) for high exudate, covered by foam. Silver dressings are not used routinely — they are reserved for wounds with confirmed local infection, for a limited two-to-four-week period.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.