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Pressure Sore (Pressure Injury)

Typical recovery: Healing time varies greatly. A superficial pressure injury may improve over days to weeks once pressure is removed and skin is protected, while Stage 3 or Stage 4 wounds can require many weeks or months of treatment. Healing is slower when perfusion, nutrition, infection control, mobility or pressure relief remain poor. Operative debridement or flap reconstruction has a separate recovery period and usually requires strict postoperative pressure avoidance before gradually returning to sitting or normal activity.

Key points

  • Pressure injury is the preferred modern term; 'pressure sore', 'bed sore' and 'pressure ulcer' are commonly used older terms.
  • Pressure injury results from pressure and often shear; moisture can worsen skin vulnerability but moisture-associated skin damage is not the same diagnosis.
  • Stage 1 has intact skin with persistent non-blanchable colour change.
  • Stage 2 is partial-thickness skin loss with exposed dermis and should not contain slough, eschar or exposed deeper tissue.
  • Stage 3 is full-thickness skin loss; fat may be visible, but fascia, muscle, tendon, cartilage and bone are not exposed.
  • Stage 4 has full-thickness skin and tissue loss with exposed or directly palpable deep structures.
  • An unstageable pressure injury has full-thickness loss whose true depth is obscured by slough or eschar.
  • Deep tissue pressure injury may present as persistent deep red, maroon or purple discolouration and can evolve rapidly.
  • Healing pressure injuries should not be reverse staged from Stage 4 to Stage 3, 2 or 1.
  • Pressure relief and repositioning are fundamental; dressings alone cannot heal a wound that remains under repeated pressure.
  • There is no evidence-based universal turning interval that is correct for every patient; repositioning must be individualised.
  • Heel off-loading should lift the heel free of the support surface rather than simply place another object directly beneath the heel.
  • Support surfaces reduce interface pressure but do not eliminate the need for skin inspection and repositioning.
  • Lower-limb perfusion should be considered before aggressive sharp debridement, especially for heel wounds.
  • Necrotic tissue often requires debridement, but a dry, stable heel eschar without signs of infection may sometimes be left intact.
  • A chronic pressure wound is commonly colonised with bacteria; colonisation alone is not an indication for systemic antibiotics.
  • Systemic antibiotics are reserved for clinical infection such as spreading cellulitis, sepsis, bacteraemia or treated osteomyelitis.
  • Exposed bone raises concern for osteomyelitis but does not by itself prove bone infection.
  • Nutrition screening and correction of protein-energy deficiency are important components of treatment.
  • Negative-pressure wound therapy can be useful for selected Stage 3 or 4 wounds after adequate debridement and infection/source control.
  • Flap reconstruction is reserved for selected patients and should follow optimisation of pressure relief, infection, nutrition and medical risk.
  • Even after successful flap closure, recurrence can occur if pressure, shear, seating or transfer problems are not corrected.
  • For frail or seriously ill patients, wound-care goals may appropriately prioritise comfort, odour control, exudate control and quality of life rather than aggressive closure.

Overview

A pressure sore, now more commonly called a pressure injury, is localised damage to the skin and/or deeper soft tissue caused by sustained or intense pressure, often combined with shear. It usually develops over a bony prominence such as the sacrum, heel, hip, ankle or elbow, but it can also occur beneath medical devices. People with limited mobility, spinal cord injury, critical illness, frailty, poor nutrition, reduced sensation or prolonged bed/chair dependence are at increased risk.

Pressure injuries are staged according to the depth and appearance of tissue damage. Stage 1 has intact skin with persistent non-blanchable colour change. Stage 2 is partial-thickness skin loss with exposed dermis. Stage 3 is full-thickness skin loss in which subcutaneous tissue may be visible. Stage 4 is full-thickness skin and tissue loss with exposed or directly palpable deeper structures such as fascia, muscle, tendon, cartilage or bone. If the true depth is obscured by slough or eschar, the wound is termed unstageable until sufficient tissue is visible. A deep tissue pressure injury can appear as persistent deep red, maroon or purple discolouration, sometimes before the full extent of injury becomes apparent. Pressure injuries should not be 'reverse staged' as they heal.

Treatment begins by removing the cause. Continued pressure on the wound delays healing, so a repositioning plan, pressure-redistributing mattress or cushion, heel off-loading and careful sitting/transfer technique are central. There is no single turning interval that is correct for every patient; frequency should reflect the patient's mobility, skin tolerance, support surface, comfort and clinical condition.

Wound care depends on stage, tissue quality, exudate, perfusion and infection risk. The wound should be cleaned gently and protected from repeated moisture, friction and contamination. Necrotic tissue usually requires debridement when it is delaying healing or contributing to infection, but debridement must be individualised. A dry, stable heel eschar without surrounding infection or inflammatory change may sometimes be left intact, particularly when perfusion is poor or the patient is not a revascularisation candidate. Arterial perfusion should be considered before aggressive debridement of lower-limb pressure injuries.

Pressure wounds are commonly colonised with bacteria; a positive swab alone does not mean that systemic antibiotics are required. Systemic antibiotics are used when there is spreading cellulitis, systemic infection, bacteraemia or confirmed/suspected osteomyelitis requiring treatment. Deep tissue or bone sampling is more useful than superficial swabs when invasive infection is suspected. Exposed or palpable bone raises concern for osteomyelitis but does not prove it by itself.

Nutrition is an important part of management. Patients at risk should be screened for malnutrition and dehydration, and protein/energy intake should be optimised when deficient. Diabetes control, anaemia, continence, spasticity, smoking and other factors that impair healing should also be addressed.

Some Stage 3 or Stage 4 wounds fail to heal despite good pressure relief, wound care and optimisation. Surgical debridement may be required for extensive devitalised tissue or infection, and selected patients may benefit from flap reconstruction after infection control, pressure-relief planning, nutritional optimisation and correction of other reversible factors. Surgery should not be viewed as a substitute for long-term pressure prevention because recurrence remains possible if the underlying pressure/shear problem continues.

Signs & symptoms

  • Persistent redness or colour change over a pressure-bearing area that does not blanch normally.
  • Pain, tenderness, warmth, coolness or altered firmness over a bony prominence.
  • A blister or shallow open wound over the sacrum, heel, hip, ankle, elbow or another pressure point.
  • A deeper crater with visible fat, slough or granulation tissue.
  • Exposed or palpable fascia, muscle, tendon, cartilage or bone in an advanced wound.
  • Dark maroon or purple skin suggesting deep tissue pressure injury.
  • Wound drainage, odour or surrounding redness when infection is present.
  • A pressure injury beneath or adjacent to a medical device such as a mask, tube, splint or catheter.
  • Reduced sensation may mean a serious pressure injury causes little or no pain.

How assessment and treatment are planned

  1. 1

    Confirm that the lesion is a pressure injury rather than moisture-associated skin damage, a skin tear, diabetic ulcer, arterial ulcer, venous ulcer or another wound type.

  2. 2

    Identify and remove the pressure/shear source, including checking bed position, wheelchair seating, footwear and medical devices.

  3. 3

    Stage the pressure injury using a recognised system and document the wound size, depth, tissue type, exudate, surrounding skin and pain.

  4. 4

    Assess mobility, sensation, continence, nutrition, hydration and comorbidities that affect healing.

  5. 5

    For lower-limb or heel wounds, assess arterial perfusion when ischaemia is possible before aggressive debridement.

  6. 6

    Create an individualised repositioning and off-loading plan and use an appropriate pressure-redistributing mattress, cushion or heel suspension device.

  7. 7

    Clean the wound gently and choose dressings that maintain an appropriate moist wound environment while managing exudate and protecting surrounding skin.

  8. 8

    Debride devitalised tissue when clinically appropriate using sharp/surgical, autolytic, enzymatic or other selected methods.

  9. 9

    Do not automatically debride a dry stable heel eschar when there are no signs of infection or instability and the clinical context favours leaving it intact.

  10. 10

    Assess for infection when there is increasing pain, erythema, warmth, purulent drainage, wound deterioration, systemic illness or unexplained failure to heal.

  11. 11

    Use systemic antibiotics for clinically invasive infection, not simply for bacterial colonisation or a positive superficial swab.

  12. 12

    Investigate suspected osteomyelitis with appropriate imaging and, when needed, deep tissue or bone sampling.

  13. 13

    Optimise protein/energy intake and correct dehydration or nutritional deficiency when identified.

  14. 14

    Optimise diabetes control, anaemia, smoking status, continence and other reversible healing barriers.

  15. 15

    Consider negative-pressure wound therapy in selected deep wounds after adequate debridement and source control.

  16. 16

    Consider operative debridement for extensive necrosis, deep infection or wounds not manageable safely at the bedside.

  17. 17

    For selected Stage 3 or Stage 4 wounds, consider flap reconstruction only after pressure relief, infection control, nutritional optimisation and a realistic long-term prevention plan are established.

Preparation

  • Bring previous wound photographs if available so progression can be assessed.
  • Bring a list of current dressings, pressure-relief devices and wound products already tried.
  • Tell the clinician how much time the patient spends in bed, chair or wheelchair and how often position changes are possible.
  • Bring details of the mattress, wheelchair cushion or heel off-loading device currently being used.
  • Mention diabetes, peripheral arterial disease, neuropathy, spinal cord injury, stroke, dementia or other mobility/sensation problems.
  • Bring recent nutrition, haemoglobin, kidney-function and glucose information if available.
  • List all antibiotics used recently and any previous wound-culture results.
  • If surgery is being considered, discuss smoking, anticoagulants, nutrition, continence, spasticity and the realistic ability to maintain postoperative pressure relief.
  • For heel or lower-limb wounds, bring prior vascular studies or revascularisation records if available.

Recovery and aftercare

  • Continue the prescribed repositioning and off-loading plan even after the wound begins to improve.
  • Inspect vulnerable pressure points daily when practical, especially the sacrum, heels, hips and areas beneath medical devices.
  • Keep skin clean and dry while protecting it from repeated urine, stool, sweat and friction.
  • Use the recommended mattress, cushion or heel suspension consistently rather than only when the wound is painful.
  • Follow dressing-change instructions and avoid repeatedly disturbing a stable wound without reason.
  • Maintain adequate protein, calories and hydration according to nutritional assessment and medical condition.
  • Continue physiotherapy, mobilisation and seating review as tolerated.
  • After surgical debridement or flap reconstruction, follow strict postoperative positioning and pressure-relief instructions.
  • Report recurrent redness, drainage, wound opening, fever or increasing pain promptly.
  • After healing, continue prevention because a previously injured area remains at higher risk of recurrence.

Risks and possible complications

  • Progression from superficial skin injury to deep tissue loss.
  • Cellulitis and soft-tissue infection.
  • Abscess formation.
  • Osteomyelitis.
  • Sepsis and organ dysfunction in severe infection.
  • Pain and sleep disturbance.
  • Chronic wound drainage and odour.
  • Bleeding during debridement or from friable tissue.
  • Loss of function and prolonged immobility.
  • Malnutrition and further physical decline during prolonged illness.
  • Need for operative debridement.
  • Need for flap reconstruction in selected deep wounds.
  • Wound breakdown or flap failure after reconstruction.
  • Recurrence if pressure and shear are not adequately controlled.
  • Prolonged healing when arterial insufficiency, diabetes, infection or severe frailty is present.

When to seek medical care

  • SOON: Persistent non-blanching redness or discolouration over a bony prominence.
  • SOON: Any new blister or open wound in a person who is bedbound, wheelchair-dependent or has reduced sensation.
  • SOON: A pressure wound that is enlarging, deepening or failing to improve despite pressure relief.
  • SOON: Black eschar, slough or increasing wound drainage.
  • SOON: Exposed or palpable bone, tendon or other deep structures.
  • SOON: New pain, malodour or increasing drainage from an existing pressure injury.
  • URGENT: Spreading redness, warmth, swelling or rapidly increasing pain around the wound.
  • URGENT: Fever, confusion, low blood pressure or other signs of sepsis.
  • URGENT: Rapidly progressive tissue necrosis, crepitus or severe pain suggesting a deeper soft-tissue infection.
  • URGENT: A pressure injury associated with uncontrolled bleeding or significant systemic deterioration.

Myth vs fact

Frequently asked questions

Sources

Medically reviewed by Dr. Shams Alam Mohammed Tahir, MBBS, MS (General Surgery). Last reviewed 2026-10-09.

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